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 468 publications

(380 citation statements)

References 45 publications

Supporting

Mentioning

337

Contrasting

Unclassified

Order By: Relevance

“…In one study, Stein et al (2007) report that high trait anxiety is associated with greater amygdala reactivity not only to angry and fearful but also happy facial expressions. Consistent with this pattern of normal variability, various mood and anxiety disorders (e.g., unipolar and bipolar depression, generalized anxiety disorder, social phobia) have been linked with greater amygdala responses to facial expressions depicting fear and anger, as well as sadness and disgust, and, more variably, to emotionally neutral facial expressions (Cooney et al 2006;Evans et al 2008;Phan et al 2006;Phillips et al 2003;Stein et al 2002;Whalen et al 2002). Such findings demonstrate that anxiety-related psychopathology is associated with a heightened amygdala response to diverse affective stimuli.…”

Section: Trait Anxiety the Amygdala And Serotoninmentioning

confidence: 84%

Toward a Mechanistic Understanding of How Variability in Neurobiology Shapes Individual Differences in Behavior

Bogdan

Carré

Hariri

2011

Current Topics in Behavioral Neurosciences

View full text Add to dashboard Cite

Research has begun to identify how variability in brain function contributes to individual differences in complex behavioral traits. Examining variability in molecular signaling pathways with emerging and established methodologies such as pharmacologic fMRI, multimodal PET/fMRI, and hormonal assays are beginning to provide a mechanistic understanding of how individual differences in brain function arise. Against this background, functional genetic polymorphisms are being utilized to understand the origins of variability in signaling pathways as well as to efficiently model how such emergent variability impacts behaviorally relevant brain function and health outcomes. This chapter provides an overview of a research strategy that integrates these complimentary levels of analysis; existing empirical data is used to illustrate the effectiveness of this approach in illuminating the mechanistic neurobiology of individual differences in complex behavioral traits. This chapter also discusses how such efforts can contribute to the identification of predictive risk markers that interact with unique environmental factors to precipitate psychopathology.

show abstract

“…Since social anxiety and sex differences have also been shown to predict the amygdala response to angry faces (McClure et al, 2004 ; Phan et al, 2006 ) we examined the influence of these factors on amygdala activity. Neither were found to independently predict the amygdala response, and all reported correlations remained significant after partialing out the effects of social anxiety (FNE) and sex differences (See Supplementary Material ).…”

Section: Resultsmentioning

confidence: 99%

“…As expected, state and trait anxiety scores were correlated ( r = 0.50, P < 0.01). Given that recent evidence has shown social anxiety influences the neural response to fearful and angry faces (Phan et al, 2006 ; Evans et al, 2007 ) we also sought to account for the influence of this dimension. Participants therefore completed the Brief Fear of Negative Evaluation (FNE) revised scale, a measure of sensitivity to negative evaluation by others and avoidance of social-evaluative situations (Carleton et al, 2006 ).…”

Section: Methodsmentioning

confidence: 99%

The interaction between gaze and facial expression in the amygdala and extended amygdala is modulated by anxiety

Ewbank¹

2010

Front. Hum. Neurosci.

View full text Add to dashboard Cite

Behavioral evidence indicates that angry faces are seen as more threatening, and elicit greater anxiety, when directed at the observer, whereas the influence of gaze on the processing of fearful faces is less consistent. Recent research has also found inconsistent effects of expression and gaze direction on the amygdala response to facial signals of threat. However, such studies have failed to consider the important influence of anxiety on the response to signals of threat; an influence that is well established in behavioral research and recent neuroimaging studies. Here, we investigated the way in which individual differences in anxiety would influence the interactive effect of gaze and expression on the response to angry and fearful faces in the human extended amygdala. Participants viewed images of fearful, angry and neutral faces, either displaying an averted or direct gaze. We found that state anxiety predicted an increased response in the dorsal amygdala/substantia innominata (SI) to angry faces when gazing at, relative to away from the observer. By contrast, high state anxious individuals showed an increased amygdala response to fearful faces that was less dependent on gaze. In addition, the relationship between state anxiety and gaze on emotional intensity ratings mirrored the relationship between anxiety and the amygdala/SI response. These results have implications for understanding the functional role of the amygdala and extended amygdala in processing signals of threat, and are consistent with the proposed role of this region in coding the relevance or significance of a stimulus to the observer.

show abstract

“…Amygdala over-reactivity elicited by implicit or non-conscious processing of threat-related stimuli has been reported in current depressive disorder [77–81] (for review, [82] ), generalized anxiety disorder [83] , generalized social phobia/anxiety disorder [83–85] , specific phobia [86] , and panic disorder [83,86] . Excessive amygdala activity elicited by masked threat faces has also been associated with a dimension of trait anxiety and with neuroticism in otherwise healthy people [87] consistent with a trait-like phenotype of hyper-reactivity to sources of threat (Table 1).…”

Section: Resultsmentioning

confidence: 99%

Defining biotypes for depression and anxiety based on large-scale circuit dysfunction: a theoretical review of the evidence and future directions for clinical translation

2016

View full text Add to dashboard Cite

Complex emotional, cognitive and self-reflective functions rely on the activation and connectivity of large-scale neural circuits. These circuits offer a relevant scale of focus for conceptualizing a taxonomy for depression and anxiety based on specific profiles (or biotypes) of neural circuit dysfunction. Here, the theoretical review first outlined the current consensus as to what constitutes the organization of large-scale circuits in the human brain identified using parcellation and meta-analysis. The focus is on neural circuits implicated in resting reflection (“default mode”), detection of “salience”, affective processing (“threat” and “reward”), “attention” and “cognitive control”. Next, the current evidence regarding which type of dysfunctions in these circuits characterize depression and anxiety disorders was reviewed, with an emphasis on published meta-analyses and reviews of circuit dysfunctions that have been identified in at least two well-powered case:control studies. Grounded in the review of these topics, a conceptual framework is proposed for considering neural circuit-defined “biotypes”. In this framework, biotypes are defined by profiles of extent of dysfunction on each large-scale circuit. The clinical implications of a biotype approach for guiding classification and treatment of depression and anxiety is considered. Future research directions will develop the validity and clinical utility of a neural circuit biotype model that spans diagnostic categories and helps to translate neuroscience into clinical practice in the real world.

show abstract

“…But even though an unavoidable confrontation with individual anxiety-laden situations is assumed to have effect on ADHD symptomatology, no causal direction between ADHD and anxiety can be stated [ 60 ]. An overall increased level of arousal as well as the tendency to hyper-focus can facilitate the development of an anxiety disorder [ 61 , 62 ]. Different studies about the comorbidity of ADHD and anxiety disorders underline these findings.…”

Section: Resultsmentioning

confidence: 99%

Developmental psychopathology: Attention Deficit Hyperactivity Disorder (ADHD)

2009

View full text Add to dashboard Cite

show abstract

“…However, a number of factors other than childhood trauma are also linked to amygdala response including sex, (Killgore and Yurgelun-Todd, 2001; Schneider et al, 2000) severity of illness, (Drevets, 2003) anxiety, (Phan et al, 2006; Etkin and Wager, 2007) adult onset trauma (Shin et al, 2005) and basal glucocorticoid activity (Drevets et al, 2002). …”

Section: Resultsmentioning

confidence: 99%

Childhood trauma history differentiates amygdala response to sad faces within MDD

Grant

Cannistraci

Hollon

et al. 2011

Journal of Psychiatric Research

149

121

View full text Add to dashboard Cite

Objective-Heightened amygdala reactivity to aversive stimuli in major depression is regarded as a core feature of the underlying physiology but individual differences in amygdala response may also arise secondary to persistent changes in limbic function during early neurodevelopment relative to stressors such as childhood trauma. We sought to determine whether heightened amygdala response is a core feature of depression or a general risk factor for psychopathology secondary to early life stress.Method-Twenty unipolar depressed patients with and without a history of significant early life trauma and 16 healthy comparison subjects underwent functional MRI in a cross-sectional study comparing neural response to sad and neutral faces.Results-We observed a robust positive correlation between physical abuse and right amygdala response. A much weaker relationship with other forms of abuse and neglect was also found, suggesting differences between abuse subtypes and amygdala response. Group differences in amygdala response suggest heightened reactivity was not characteristic of persons with depression in general but was true primarily in those with a significant history of abuse.Conclusion-These findings suggest the relationship between childhood trauma and risk for depression is mediated by heightened amygdala response but varies by abuse type. Preliminary evidence for two distinct depression phenotypes based on trauma history was also supported, consistent with differential etiology.Keywords childhood trauma; amygdala; stress sensitization; depression Major depressive disorder is a serious illness estimated to affect 13 to 14 million adults annually and approximately 16% of the U.S. population across the lifespan (Kessler et al., 2003). Furthermore, the considerable social, occupational and workplace related costs associated with impaired function are estimated in the tens of billions of dollars each year (Wang et al., 2006). Childhood maltreatment has emerged as a significant risk factor for the onset of adult depression with over 500,000 documented cases of physical and sexual abuse © 2010 Elsevier Ltd. All rights reserved. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. (Sedlak et al., 2010). Despite the widely appreciated magnitude of the problem, the precise mechanism by which childhood trauma may increase the risk for depression remains unclear. NIH Public AccessExaggerated amygdala response is regarded as a core feature of the underlying physiology of unipolar depression (Price and Drevets, 2010). Imaging studies utilizing both positron emission tomography (PET)...

show abstract

“…A total of 1297 publications were retrieved from initial search, among which 37 studies met the inclusion criteria (654 participants in the SAD groups and 594 participants in the control groups). There were 15 studies that adopted emotional faces as task stimuli [ 6 , 10 , 13 , 14 , 15 , 16 , 17 , 18 , 19 , 20 , 21 , 22 , 23 , 24 , 25 ], 8 that presented specific situations as task stimuli [ 26 , 27 , 28 , 29 , 30 , 31 , 32 , 33 ], and the other 14 employed other types of tasks [ 7 , 34 , 35 , 36 , 37 , 38 , 39 , 40 , 41 , 42 , 43 , 44 , 45 , 46 ]. In total, the coordinates where SAD groups performed significantly better or significantly worse than control groups were 335 and 115 respectively (see specific characteristics in Table 1 ).…”

Section: Resultsmentioning

confidence: 99%

Cognitive Neural Mechanism of Social Anxiety Disorder: A Meta-Analysis Based on fMRI Studies

Ruan

Yawen

et al. 2021

IJERPH

View full text Add to dashboard Cite

Objective: The present meta-analysis aimed to explore the cognitive and neural mechanism of social anxiety disorder (SAD) from a whole-brain view, and compare the differences in brain activations under different task paradigms. Methods: We searched Web of Science Core Collection and other databases with the keywords related to social anxiety, social phobia, and functional magnetic resonance imaging (fMRI) for comparing persons with SAD to healthy controls and used the activation likelihood estimation method. Thirty-seven papers met the inclusion criteria, including 15 with emotional faces as stimuli, 8 presenting specific situations as stimuli, and 14 using other types of tasks as stimuli. Among these papers, 654 participants were in the SAD group and 594 participants were in the control group with 335 activation increase points and 115 activation decrease points. Results: Whole-brain analysis showed that compared with healthy controls, persons with SAD showed significantly lower activation of the left anterior cingulate gyrus (MNI coordinate: x = −6, y = 22, z = 38; p < 0.001). Sub-group analysis based on task indicated that when performing tasks with emotional faces as stimuli, persons with SAD showed significantly lower activation of the left cerebellar slope and fusiform gyrus (MNI coordinate: x = −26, y = −68, z = −12; p < 0.001), and significantly higher activation of the right supramarginal gyrus and angular gyrus, than healthy controls (MNI coordinate: x = 58, y = −52, z = 30; p < 0.001). Conclusion: Individuals with social anxiety disorder show abnormal activation in the cingulate gyrus, which is responsible for the process of attention control, and task type can influence the activation pattern.

show abstract

“…Task Activations. The EFMT is designed to detect between group differences in amygdala activity, [10,14] and thus, we restrict our report of activations to between group results. gSAD patients showed greater right amygdala activity than HCs in the fearful versus happy faces contrast (P < .05, cluster extent > 200 voxels).…”

Section: Functional Mri Resultsmentioning

confidence: 99%

“…Evidence of a link between amygdala hyperactivity and symptom severity suggests it is a core deficit in the pathophysiology of gSAD [10] . Although less commonly implicated [11] , abnormalities within the prefrontal cortex (PFC) are hypothesized to underlie gSAD patients’ failure to effectively modulate amygdala reactivity, consequently leading to enhanced anxiety, social threat perception, and/or reticence to engage in social interactions [12] .…”

Section: Introductionmentioning

confidence: 99%

“…Although less commonly implicated [11] , abnormalities within the prefrontal cortex (PFC) are hypothesized to underlie gSAD patients’ failure to effectively modulate amygdala reactivity, consequently leading to enhanced anxiety, social threat perception, and/or reticence to engage in social interactions [12] . Consistent with this hypothesis, gSAD patients show atypical reactivity to the detection of social signals of threat in areas such as the anterior cingulate cortex (ACC) [10; 13] , and dorsal and ventral medial PFC (mPFC) [14] . Given their strong reciprocal structural connections with the amygdala [15] , discrete areas of the PFC are well-positioned to play a significant role in the regulation of fear and emotional responding.…”

Section: Introductionmentioning

(Expert classified)

“…[9] Evidence of a link between amygdala hyperactivity and symptom severity suggests it is a core deficit in the pathophysiology of gSAD. [10] Although less commonly implicated, [11] abnormalities within the prefrontal cortex (PFC) are hypothesized to underlie gSAD patients' failure to effectively modulate amygdala reactivity, consequently leading to enhanced anxiety, social threat perception, and/or reticence to engage in social interactions. [12] Consistent with this hypothesis, gSAD patients show atypical reactivity to the detection of social signals of threat in areas such as the anterior cingulate cortex (ACC), [10,13] and dorsal and ventral medial PFC (mPFC).…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Aberrant Amygdala-Frontal Cortex Connectivity During Perception of Fearful Faces and at Rest in Generalized Social Anxiety Disorder

et al. 2012

View full text Add to dashboard Cite

Background Generalized social anxiety disorder (gSAD) is characterized by exaggerated amygdala reactivity to social signals of threat, but if and how the amygdala interacts with functionally and anatomically connected prefrontal cortex (PFC) remains largely unknown. Recent evidence points to aberrant amygdala connectivity to medial PFC in gSAD at rest, but it is difficult to attribute functional relevance without the context of threat processing. Here, we address this by studying amygdala-frontal cortex connectivity during viewing of fearful faces and at rest in gSAD patients. Methods Twenty patients with gSAD and 17 matched healthy controls (HCs) participated in functional magnetic resonance imaging of an emotional face matching task, and a resting state task. Functional connectivity and psychophysiological interaction analysis were used to assess amygdala connectivity. Results Compared to HCs, gSAD patients exhibited less connectivity between amygdala and the rostral anterior cingulate cortex (ACC) and dorsolateral prefrontal cortex (DLPFC) while viewing fearful faces. gSAD patients also showed less connectivity between amygdala and rostral ACC at rest in the absence of fearful faces. DLPFC connectivity was negatively correlated with LSASFear. Conclusions Task and rest paradigms provide unique and important information about discrete and overlapping functional networks. In particular, amygdala coupling to DLPFC may be a phasic abnormality, emerging only in the presence of a social predictor of threat, whereas amygdala coupling to the rostral ACC may reflect both phasic and tonic abnormalities. These findings prompt further studies to better delineate intrinsic and externally-evoked brain connectivity in anxiety and depression in relation to amygdala dysfunction.

show abstract

“…Although it has been argued that fear and anger are avoidance‐ and approach‐related emotions, respectively, they are both conceptualized as threat‐related emotions and previous research has shown links between shyness and threat‐related biases in children (e.g., LoBue & Pérez‐Edgar, ; Muris, Merckelbach, & Damsma, ; Pérez‐Edgar et al, ). Neuroimaging studies provide further support of both anger and fear being conceptualized as threat‐related emotions, with each being associated with heightened amygdala activity, a key brain region implicated in social and threat‐processing and perception (e.g., Etkin & Wager, ; Klumpp, Angstadt, Nathan, & Phan, ; Phan, Fitzgerald, Nathan, & Tancer, ).…”

Section: Methodsmentioning

confidence: 90%

Trajectory of heart period to socioaffective threat in shy children

Poole

2018

Developmental Psychobiology

View full text Add to dashboard Cite

Although shyness is characterized by distinct psychophysiological correlates, we know very little about the development of these correlates. In this longitudinal study, we examined how children's shyness was associated with trajectories of heart period (HP) to socioaffective threat across four assessments spanning approximately 2 years. Children (M = 6.39 years) viewed age-appropriate, socioaffective videos at each visit while having their HP measured concurrently. A growth curve analysis revealed that low shy children had a relatively lower HP at enrollment, but experienced increases in HP across visits, while high shy children exhibited relatively stable low HP across visits while viewing threat-related socioaffective video stimuli. These patterns did not exist for HP during resting baseline or HP to nonthreatening video stimuli. These findings suggest that longitudinal patterns of HP among shy children may reflect a stable, characteristic way of responding to socioaffective threat, and possibly a physiological mechanism underlying shyness in some children.

show abstract

“…The possible reorganization of the sensory visual cortex correspondent to alterations in motivational thresholds associated with excessive social apprehension is supported by animal and human work revealing that the functional neuroarchitecture of the adult visual cortex is subject to changes related to behavioral contingencies (Karmarkar & Dan, 2006; Li et al, 2004) and re-entrant modulation from higher visual areas including temporal cortex and deep structures such as the amygdala (Damasio, 1998; Leppänen & Nelson, 2009; Sabatinelli et al, 2005; 2009)—areas consistently shown during functional neuroimaging to be hyper-reactive to facial stimuli in social phobia patients (Birbaumer et al, 1998; Evans et al, 2008; Phan et al, 2006; Schneider et al, 1999; Stein et al, 2002; Straube et al, 2004, Veit et al, 2002). Although speculative, the heightened attention to emotional faces may be the result of visual system plasticity secondary to chronic expectations of interpersonal failure typical of social anxiety (Andrews et al, 1994; Foa et al, 1996; Poulton & Andrews, 1996; Rapee & Heimberg, 1997).…”

Section: Discussionmentioning

confidence: 96%

“…Although heightened sensitivity specific to angry expressions would seem most consistent with the nosology of social anxiety, vigilance to other expressions has frequently been revealed in both ERP (Kolassa et al, 2007; 2009; Wieser et al, 2010) and hemodynamic imaging (Amir et al, 2005, Birbaumer et al, 1998; Phan et al, 2006; Stein et al, 2002) studies—even to happy faces (Yoon et al, 2007; Straube et al, 2005) and aversive non-social scenes (Shah et al, 2009). Much of the evidence for exaggerated reactivity to “harsh” facial expressions has been demonstrated as the mean response to heterogeneous aversive displays (angry, fearful, disgusted) (e.g., Moser et al, 2008; Phan et al, 2006; Stein et al, 2002).…”

Section: Discussionmentioning

confidence: 99%

“…Much of the evidence for exaggerated reactivity to “harsh” facial expressions has been demonstrated as the mean response to heterogeneous aversive displays (angry, fearful, disgusted) (e.g., Moser et al, 2008; Phan et al, 2006; Stein et al, 2002). In post hoc tests of the BOLD response to individual aversive contents, Phan and colleagues revealed that the overall effect was attributable to reliable, similar magnitude amygdala activity to angry, fearful and disgusted faces.…”

Section: Discussionmentioning

confidence: 99%

“…Concerning neurophysiological underpinnings, hemodynamic imaging studies have revealed that relative to controls socially anxious individuals and patients show exaggerated activation of limbic circuitry, particularly amygdala (Birbaumer et al, 1998; Evans et al, 2008; Phan et al, 2006; Schneider et al, 1999; Stein et al, 2002; Straube et al, 2004, 2005; Veit et al, 2002), in response to emotional facial expressions, again presented for a wide range of durations (i.e., 100 ms – 2500 ms). Less frequently an a priori area of interest, concurrent hyper-reactivity has also been observed in the extrastriate visual cortex (Evans et al, 2008; Goldin et al, 2009; Pujol et al, 2009; Straube et al, 2004; 2005).…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Social vision: Sustained perceptual enhancement of affective facial cues in social anxiety

et al. 2011

View full text Add to dashboard Cite

Heightened perception of facial cues is at the core of many theories of social behavior and its disorders. In the present study, we continuously measured electrocortical dynamics in human visual cortex, as evoked by happy, neutral, fearful, and angry faces. Thirty-seven participants endorsing high versus low generalized social anxiety (upper and lower tertiles of 2,104 screened undergraduates) viewed naturalistic faces flickering at 17.5 Hz to evoke steady-state visual evoked potentials (ssVEPs), recorded from 129 scalp electrodes. Electrophysiological data were evaluated in the time-frequency domain after linear source space projection using the minimum norm method. Source estimation indicated an early visual cortical origin of the face-evoked ssVEP, which showed sustained amplitude enhancement for emotional expressions specifically in individuals with pervasive social anxiety. Participants in the low symptom group showed no such sensitivity, and a correlational analysis across the entire sample revealed a strong relationship between self-reported interpersonal anxiety/avoidance and enhanced visual cortical response amplitude for emotional, versus neutral expressions. This pattern was maintained across the 3500 ms viewing epoch, suggesting that temporally sustained, heightened perceptual bias towards affective facial cues is associated with generalized social anxiety.

show abstract

“…On the whole, these studies failed to find a consistent association between BIS/trait anxiety scores and autonomic responses to stimuli or tasks designed to activate the BIS [26,30,[35][36][37][38][39]48,51]. In addition to the evidence of dissociation between BI and trait anxiety on the one hand and the amygdala on the other, there is evidence of neural dissociation between BI and trait anxiety.…”

Section: Discussionmentioning

confidence: 96%

“…No or inconsistent correlations between CW-BIS, SP(SR)Q, and STAI-T and hypothesized neural substrates of the BIS (ie, amygdala) as indexed by SCL and SR is therefore a relatively consistent finding (see also [38,39]) and may expose a lack of sensitivity/specificity in these self-report measures of BIS temperament. The suggestion that STAI-T is more sensitive to affective tone and physiologic output of the BIS than the CW-BIS scale [30] is not consistent with the data of Cornwell et al [37], which showed that STAI-T did not correlate with SCL or SR at baseline or during speech performance.…”

Section: Neurobiologymentioning

confidence: 88%

“…Several recent studies investigated the biological correlates of the BIS and trait anxiety as measured by a variety of self-report scales [26,30,[35][36][37][38][39]48,51]. On the whole, these studies failed to find a consistent association between BIS/trait anxiety scores and autonomic responses to stimuli or tasks designed to activate the BIS [26,30,[35][36][37][38][39]48,51].…”

Section: Discussionmentioning

confidence: 99%

“…Operationally, this has entailed the use of self-report "BIS" scales possibly lacking in specificity and sensitivity, as well as the use of experimental paradigms and fear-inducing stimuli that appear to be too nonspecific. For example, factors such as social versus nonsocial anxiety [30,37,38], temperament-valence interactions [36], or attentional demands [51] appear to be exerting significant confounding effects. There also has been, with few exceptions [50••,53••], a failure to consider cortical or subcortical substrates of BI and trait anxiety other than the amygdala.…”

Section: Discussionmentioning

confidence: 99%

“…Of possible interest in this regard, Cornwell et al [37] found that subjective state anxiety (measured by STAI-State) correlated with FNE, SSPS, and STAI-T (but not SR) during speech, suggesting that neither "general" trait nor "general" state anxiety mediates the correlation between trait social anxiety and SR found by these authors. Phan et al [38] also recently reported on a functional MRI (fMRI) study that found significant amygdala hyperactivation to aversive (anger/disgust/fear) facial expressions in 10 subjects with generalized social phobia (GSP), whereas 10 healthy controls subjects showed slight deactivation. The results confirmed several previous studies but also revealed a significant correlation between the blood oxygen level-dependent signal change and symptom severity in the GSP group as measured by the Liebowitz Social Anxiety Scale.…”

Section: Neurobiologymentioning

confidence: 91%

“…Taken together, these studies suggest a link between social anxiety as distinct from general trait anxiety and physiologic responsiveness. In addition, the failure to find an association between general trait anxiety and SR in a speech task [37], as well as the observation of amygdala deactivation to aversive stimuli in normal controls [38], is yet more evidence of a dissociation between these kinds of anxiogenic stimuli, which theoretically should activate the BIS and this brain structure. Questions about the validity of self-report measures of BIS temperament are echoed by Cogswell et al [24], who caution against the unqualified use of self-report scales, emphasizing both the need to improve their validity and investigate their behavioral correlates in order to properly examine their theoretical bases.…”

Section: Neurobiologymentioning

confidence: 98%

See 4 more Smart Citations

Behavioral inhibition: A neurobiological perspective

Morgan

2006

Curr Psychiatry Rep

View full text Add to dashboard Cite

Behavioral inhibition (BI) during early childhood has been associated with subsequent development of anxiety disorders. However, understanding of the neuroanatomical substrates of BI in humans generally has not kept pace with that of anxiety disorders. Recent interpretations and implementations of Gray's and Kagan's concepts of BI are examined from the perspective of current neurobiological models. Particular attention is given to evidence pointing to conceptual and operational limitations of self-report scales purported to measure trait BI in adults, and especially to inconsistent correlations between such behavioral inhibition system (BIS) scores and amygdala and autonomic responses to fear- or startle-inducing stimuli. Evidence showing a dissociation of both BI and trait anxiety from the amygdala is considered. Possible reasons for the poor association between BIS and trait anxiety self-report scale scores and predicted physiological outputs of the BIS are identified. Reasons to distinguish between the neural bases of BI as against trait anxiety also are discussed. The need to critically examine the role of the amygdala in BI and trait anxiety, as well as to consider other brain areas that appear to be involved in subserving these emotional traits, is emphasized.

show abstract

1 2 3 4 5 678 9 10

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

Cited by 468 publications

References 45 publications

Toward a Mechanistic Understanding of How Variability in Neurobiology Shapes Individual Differences in Behavior

The interaction between gaze and facial expression in the amygdala and extended amygdala is modulated by anxiety

Defining biotypes for depression and anxiety based on large-scale circuit dysfunction: a theoretical review of the evidence and future directions for clinical translation

Developmental psychopathology: Attention Deficit Hyperactivity Disorder (ADHD)

Childhood trauma history differentiates amygdala response to sad faces within MDD

Cognitive Neural Mechanism of Social Anxiety Disorder: A Meta-Analysis Based on fMRI Studies

Aberrant Amygdala-Frontal Cortex Connectivity During Perception of Fearful Faces and at Rest in Generalized Social Anxiety Disorder

Trajectory of heart period to socioaffective threat in shy children

Social vision: Sustained perceptual enhancement of affective facial cues in social anxiety

Behavioral inhibition: A neurobiological perspective

Contact Info

Product

Resources

About