Brain activation to phobia-related words in phobic subjects

Straube, Thomas; Mentzel, Hans Joachim; Glauer, Madlen; Miltner, Wolfgang H. R.

doi:10.1016/j.neulet.2004.09.050

Cited by 63 publications

(42 citation statements)

References 25 publications

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“…It was showed that anterior part of insula is activated during exposition of fearful stimuli (Critchley et al 2002) and that it plays a key role in the process of threat overestimating in subjects with anxiety disorders (Lorberbaum et al 2004, Straube et al 2004a, 2004b. It is possible that elevated activity in this area in the study group was caused by evaluating neutral feedback stimuli as threatening.…”

Section: Discussionmentioning

confidence: 96%

“…It has been previously presented that anterior cingulate cortex is involved in attentional and emotional processes, detection of relevant stimuli and it is important part of cortico-subcortical loop involved in fear conditioning (Eser et al 2009, Javanmard et al 1999, Jensen et al 2003, Ketter et al 1996, Klumpp et al 2014, Phelps et al 2004, Schunck et al 2006, Servan-Schreiber et al 1998, Straube et al 2010. It was shown that anterior cingulate cortex is involved in pathophysiology of anxiety disorder, usually manifested by elevated activity (Bremner et al 2005, Brühl et al 2014, Dilger and Straube 2003, Klumpp et al 2014, Kopřivova et al 2011, Lorberbaum et al 2004, McClure et al 2007, Monk et al 2008, Nitschke et al 2009, Saxena and Rauch 2000, Straube et al 2004a, 2004b, Wright et al 2003, although it was also shown that after exposition of incongruent stimulus subjects with anxiety disorders had smaller activity in anterior cingulate cortex (Etkin et al 2010). The increase of activity in anterior cingulate cortex and anterior part of insula in subjects with anxiety disorders often correlates with elevated activity in amygdala (Brühl et al 2014, Shin andLiberzon 2010).…”

Section: Discussionmentioning

confidence: 99%

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EEG source activity during processing of neutral stimuli in subjects with anxiety disorders

Gmaj¹,

Januszko²,

Kamiński³

et al. 2016

Acta Neurobiologiae Experimentalis

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Anxiety disorders are a social problem due to their prevalence and consequences. It is crucial to explore the influence of anxiety on cognitive processes. In this study we recorded EEG activity from 73 subjects (35 patients, 38 controls, matched for age and education) during performance of the Continuous Attention Task. We used low resolution electromagnetic tomography (LORETA) for evaluation of mechanisms of impaired cognitive performance in anxiety disorders. Analysis showed that patients with anxiety disorders committed more errors than the controls, had a short latency of P300 and higher amplitude of ERPs at all steps of stimulus processing. Furthermore, we showed that there was a relationship between the scores of Hamilton Anxiety Scale and Beck Depression Inventory, and amplitudes and latencies of ERPs. The results of LORETA analysis showed that enhanced neural responses were found within circuits mediating visual information processing, sustained attention and anxiety. Also, we found higher current density within areas playing an important role in the brain fear network -anterior cingulate and anterior part of insula. Electrophysiological neuroimaging showed greater recruitment of cognitive resources in anxiety disorders, evidenced by higher current density and activation of greater number of brain areas. Despite the strategy employed to compensate for cognitive problems, the anxiety patients did not achieve the same performance as controls. Present study demonstrates that anxiety disorders influence processing of neutral stimuli and this influence is observable at both behavioral and electrophysiological level. The data suggests instability of neural systems responsible for information selection, working memory, engagement and focusing of attention.

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Section: Discussionmentioning

confidence: 96%

Section: Discussionmentioning

confidence: 99%

EEG source activity during processing of neutral stimuli in subjects with anxiety disorders

Gmaj¹,

Januszko²,

Kamiński³

et al. 2016

Acta Neurobiologiae Experimentalis

View full text Add to dashboard Cite

show abstract

“…Similarly, although many studies have reported increases in amygdalar activity in specific phobia, several studies have reported no patient/comparison subject differences (33)(34)(35), and one reported decreased amygdala activation in patients (36). Finally, in panic disorder and OCD, amygdalar hyperactivity appears to be the exception, rather than the rule (37,38).…”

mentioning

confidence: 98%

Functional Neuroimaging of Anxiety: A Meta-Analysis of Emotional Processing in PTSD, Social Anxiety Disorder, and Specific Phobia

Etkin¹,

Wager²

2007

AJP

2,957

172

2,306

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Objective-The study of human anxiety disorders has benefited greatly from functional neuroimaging approaches. Individual studies, however, vary greatly in their findings. The authors searched for common and disorder-specific functional neurobiological deficits in several anxiety disorders. The authors also compared these deficits to the neural systems engaged during anticipatory anxiety in healthy subjects.Method-Functional magnetic resonance imaging and positron emission tomography studies of posttraumatic stress disorder (PTSD), social anxiety disorder, specific phobia, and fear conditioning in healthy individuals were compared by quantitative meta-analysis. Included studies compared negative emotional processing to baseline, neutral, or positive emotion conditions.Results-Patients with any of the three disorders consistently showed greater activity than matched comparison subjects in the amygdala and insula, structures linked to negative emotional responses. A similar pattern was observed during fear conditioning in healthy subjects. Hyperactivation in the amygdala and insula were, of interest, more frequently observed in social anxiety disorder and specific phobia than in PTSD. By contrast, only patients with PTSD showed hypoactivation in the dorsal and rostral anterior cingulate cortices and the ventromedial prefrontal cortex-structures linked to the experience and regulation of emotion.Conclusions-This meta-analysis allowed us to synthesize often disparate findings from individual studies and thereby provide neuroimaging evidence for common brain mechanisms in anxiety disorders and normal fear. Effects unique to PTSD furthermore suggested a mechanism for the emotional dysregulation symptoms in PTSD that extend beyond an exaggerated fear response. Therefore, these findings help refine our understanding of anxiety disorders and their interrelationships.Fear and avoidance of trigger cues are common to many anxiety disorders (1) and resemble the arousal and avoidance responses shown by normal subjects to conditioned fear cues (2). Thus, a common element of anxiety disorders may be an abnormally elevated fear response. Based on animal models of fear learning (3, 4), this hypothesis leads to the prediction that amygdalar dysfunction is common to a variety of anxiety disorders. Indeed, amygdalar hyperactivity has been observed during symptom provocation or negative emotional processing in patients with posttraumatic stress disorder (PTSD) (5-8), social anxiety disorder (9-14), specific phobia (15-18), panic disorder (19), and obsessive-compulsive disorder (OCD) (19,20). However, because of the low statistical power of individual studies Address correspondence and reprint requests to Dr. Etkin, Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, 401 Quarry Rd., Stanford, CA 94305; amitetkin@stanford.edu. All authors report no competing interests. NIH Public Access Author ManuscriptAm J Psychiatry. Author manuscript; available in PMC 2012 April 4. NIH-PA Author Manuscr...

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“…Both disorders have been related to increased amygdala responsiveness. Thus, a core feature of generalized social phobia is atypically increased responses to other individuals' emotional expressions in regions of the brain, including the amygdala, the anterior cingulate cortex, and the extrastriate cortex (9)(10)(11)(12)(13)(14)(15)(16)(17). The empirical picture is less clear in generalized anxiety disorder.…”

mentioning

confidence: 99%

Response to Emotional Expressions in Generalized Social Phobia and Generalized Anxiety Disorder: Evidence for Separate Disorders

Blair¹,

Shaywitz²,

Smith³

et al. 2008

AJP

257

248

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Objective-Generalized social phobia involves fear/avoidance, specifically of social situations, whereas generalized anxiety disorder involves intrusive worry about diverse circumstances. It remains unclear the degree to which these two, often comorbid, conditions represent distinct disorders or alternative presentations of a single, core underlying pathology. Functional magnetic resonance imaging assessed the neural response to facial expressions in generalized social phobia and generalized anxiety disorder.Method-Individuals matched on age, IQ, and gender with generalized social phobia without generalized anxiety disorder (N=17), generalized anxiety disorder (N= 17), or no psychopathology (N=17) viewed neutral, fearful, and angry expressions while ostensibly making a simple gender judgment.Results-The patients with generalized social phobia without generalized anxiety disorder showed increased activation to fearful relative to neutral expressions in several regions, including the amygdala, compared to healthy individuals. This increased amygdala response related to selfreported anxiety in patients with generalized social phobia without generalized anxiety disorder. In contrast, patients with generalized anxiety disorder showed significantly less activation to fearful relative to neutral faces compared to the healthy individuals. They did show significantly increased response to angry expressions relative to healthy individuals in a lateral region of the middle frontal gyrus. This increased lateral frontal response related to self-reported anxiety in patients with generalized anxiety disorder.Conclusions-These results suggest that neural circuitry dysfunctions differ in generalized social phobia and generalized anxiety disorder.Generalized social phobia and generalized anxiety disorder are two highly prevalent, chronic, and disabling anxiety disorders (1,2) that are sometimes comorbid. Generalized social phobia involves fear/avoidance, specifically of social situations, whereas generalized anxiety disorder involves intrusive worry about a broader array of everyday life circumstances. Although both have considerable social and economic costs, disagreement exists concerning the degree to which the conditions result from a shared or unique pathophysiology. For example, high rates of comorbidity in cross-sectional and longitudinal studies suggest that the distinction between the two conditions may be relatively subtle at the descriptive level (3,4). On the other hand, data from family-based and therapeutic research suggest the two conditions can be dissociated. Specifically, such dissociation is reflected in patterns of disorder aggregation within families (5), as well as by the fact that generalized anxiety disorder, but not social phobia, responds to most tricyclic antidepressants and to buspirone (6-8). Because no brain-imaging study has directly compared the two conditions, it remains unclear whether the two disorders have dissociable neural correlates.The principal goal of the current study was to inves...

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Brain activation to phobia-related words in phobic subjects

Cited by 63 publications

References 25 publications

EEG source activity during processing of neutral stimuli in subjects with anxiety disorders

EEG source activity during processing of neutral stimuli in subjects with anxiety disorders

Functional Neuroimaging of Anxiety: A Meta-Analysis of Emotional Processing in PTSD, Social Anxiety Disorder, and Specific Phobia

Response to Emotional Expressions in Generalized Social Phobia and Generalized Anxiety Disorder: Evidence for Separate Disorders

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