Development of anxiety: The role of threat appraisal and fear learning

Mood and Anxiety Disorders Program, National Institute of Mental Health, 9000 Rockville Pike, Bethesda, MD 20892, USA.
Depression and Anxiety (Impact Factor: 4.41). 01/2011; 28(1):5-17. DOI: 10.1002/da.20733
Source: PubMed


Anxious individuals exhibit threat biases at multiple levels of information processing. From a developmental perspective, abnormal safety learning in childhood may establish threat-related appraisal biases early, which may contribute to chronic disorders in adulthood. This review illustrates how the interface among attention, threat appraisal, and fear learning can generate novel insights for outcome prediction. This review summarizes data on amygdala function, as it relates to learning and attention, highlights the importance of examining threat appraisal, and introduces a novel imaging paradigm to investigate the neural correlates of threat appraisal and threat-sensitivity during extinction recall. This novel paradigm can be used to investigate key questions relevant to prognosis and treatment. Depression and Anxiety, 2011.© 2010 Wiley-Liss, Inc.

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    • "In essence, appraisal establishes the personal relevance of environmental stimuli according to the individual's concern for well-being, based on needs, goals, and beliefs [53] [20]. 'Threat appraisal' therefore denotes classifying a stimulus based on its capacity for harming the organism [9]. A possible negative outcome of this adaptive mechanism, having evolved to assist effective threat detection [29], is that threat cues can take on excessive salience, creating a hyper-vigilance or attentional bias towards threat [28] [2]. "
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    ABSTRACT: A key factor in the transition to psychosis is the appraisal of anomalous experiences as threatening. Cognitive models of psychosis have identified attentional and interpretative biases underlying threat-based appraisals. While much research has been conducted into these biases within the clinical and cognitive literature, little examination has occurred at the neural level. However, neurobiological research in social cognition employing threatening stimuli mirror cognitive accounts of maladaptive appraisal in psychosis. This review attempted to integrate neuroimaging data regarding social cognition in psychosis with the concepts of attentional and interpretative threat biases. Systematic review methodology was used to identify relevant articles from Medline, PsycINFO and EMBASE, and PubMed databases. The selective review showed that attentional and interpretative threat biases relate to abnormal activation of a range of subcortical and prefrontal structures, including the amygdala, insula, hippocampus, anterior cingulate, and prefrontal cortex, as well as disrupted connectivity between these regions, when processing threatening and neutral or ambiguous stimuli. Notably, neural findings regarding the misattribution of threat to neutral or ambiguous stimuli presented a more consistent picture. Overall, however, the findings for any specific emotion were mixed, both in terms of the specific brain areas involved and the direction of effects (increased/decreased activity), possibly owing to confounds including small sample sizes, varying experimental paradigms, medication, and heterogeneous, in some cases poorly characterised, patient groups. Further neuroimaging research examining these biases by employing experimentally induced anomalous perceptual experiences and well-characterised large samples is needed for greater aetiological specificity.
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    • "Another bias that is introduced into this loop of decisions and predictions is attentional bias. It is well documented that people with anxiety disorders show enhanced threat detection, persistently pay more attention to these stimuli, and show a bias in threat appraisal (Britton et al. 2011). Although the role of the hippocampus in this attention bias is not clear, such a role does seem consistent with hippocampal function in orienting, attention, and persistence, as discussed above. "

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    • "Furthermore, medial prefrontal cortex represents the biological relevance of a given stimulus and may convey this information to the dorso-lateral prefrontal cortex (Mechias et al., 2010). Amygdala may play a pivotal role in the learning processes related to emotional reactions, fear, and fear extinction (Phelps et al., 2004; Milad et al., 2009; Britton et al., 2011). Secondly, positive functional connectivity was found in PTSD patients between the amygdala and anterior cingulate cortex in response to stimulations related to emotionally traumatic stimuli (Osuch et al., 2008) and during the observation of fearful faces under anxious conditions in healthy subjects (Robinson et al., 2012). "
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    ABSTRACT: Patients with post-traumatic stress disorder (PTSD) tend to misinterpret innocuous stimuli as potential threats, possibly due to a conditioning provoked by traumatic episodes. Previous neuroimaging evidence has shown an abnormal activation of the amygdala and prefrontal cortex in PTSD patients during fear conditioning and extinction. Nevertheless, the effects of a single-type adverse stressor on that circuit remain poorly explored. We tested the hypothesis that a single-type adverse episode is able to affect the prefrontal cortex and amygdala response to conditioned stimuli. To test this hypothesis, fMRI recordings were performed in PTSD patients and trauma-exposed controls during the observation of neutral and negative paired or non-paired pictures with an adverse stimulus by means of a single association. Results showed that left amygdala activation during negative reinforced stimuli was correlated with the score of PTSD clinical scale across all subjects. Furthermore, in the traumatized non-PTSD group, the activation of the dorso-medial prefrontal cortex and bilateral amygdala was lower during the observation of the reinforced (CS(+)) vs non-reinforced pictures (CS(-)) in response to emotionally negative stimuli. This was not the case in the PTSD patients. These results suggest that in PTSD patients, a single-episode conditioning unveils the failure of an inhibitory mechanism moderating the activity of the prefrontal cortex and amygdala in response to adverse and neutral stimuli. Copyright © 2015. Published by Elsevier Inc.
    Brain research bulletin 03/2015; 114. DOI:10.1016/j.brainresbull.2015.03.001 · 2.72 Impact Factor
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