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      Social anxiety disorder in adolescence: How developmental cognitive neuroscience findings may shape understanding and interventions for psychopathology


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          • Late childhood and adolescence are a sensitive juncture for social anxiety onset.

          • Cognitive biases linked to social anxiety manifest in differences in functional brain response.

          • Normative socio-affective developments may exacerbate biased processing.

          • Increased plasticity/learning may make adolescence an ideal time to intervene.

          • Modifying processing biases through cognitive training and neurofeedback represent two possible age-appropriate interventions.


          Social anxiety disorder represents a debilitating condition that has large adverse effects on the quality of social connections, educational achievement and wellbeing. Age-of-onset data suggests that early adolescence is a developmentally sensitive juncture for the onset of social anxiety. In this review, we highlight the potential of using a developmental cognitive neuroscience approach to understand (i) why there are normative increases in social worries in adolescence and (ii) how adolescence-associated changes may ‘bring out’ neuro-cognitive risk factors for social anxiety in a subset of individuals during this developmental period. We also speculate on how changes that occur in learning and plasticity may allow for optimal acquisition of more adaptive neurocognitive strategies through external interventions. Hence, for the minority of individuals who require external interventions to target their social fears, this enhanced flexibility could result in more powerful and longer-lasting therapeutic effects. We will review two novel interventions that target information-processing biases and their neural substrates via cognitive training and visual feedback of neural activity measured through functional magnetic resonance imaging.

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          Most cited references118

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          Resolving emotional conflict: a role for the rostral anterior cingulate cortex in modulating activity in the amygdala.

          Effective mental functioning requires that cognition be protected from emotional conflict due to interference by task-irrelevant emotionally salient stimuli. The neural mechanisms by which the brain detects and resolves emotional conflict are still largely unknown, however. Drawing on the classic Stroop conflict task, we developed a protocol that allowed us to dissociate the generation and monitoring of emotional conflict from its resolution. Using functional magnetic resonance imaging (fMRI), we find that activity in the amygdala and dorsomedial and dorsolateral prefrontal cortices reflects the amount of emotional conflict. By contrast, the resolution of emotional conflict is associated with activation of the rostral anterior cingulate cortex. Activation of the rostral cingulate is predicted by the amount of previous-trial conflict-related neural activity and is accompanied by a simultaneous and correlated reduction of amygdalar activity. These data suggest that emotional conflict is resolved through top-down inhibition of amygdalar activity by the rostral cingulate cortex.
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            Peers increase adolescent risk taking by enhancing activity in the brain's reward circuitry.

            The presence of peers increases risk taking among adolescents but not adults. We posited that the presence of peers may promote adolescent risk taking by sensitizing brain regions associated with the anticipation of potential rewards. Using fMRI, we measured brain activity in adolescents, young adults, and adults as they made decisions in a simulated driving task. Participants completed one task block while alone, and one block while their performance was observed by peers in an adjacent room. During peer observation blocks, adolescents selectively demonstrated greater activation in reward-related brain regions, including the ventral striatum and orbitofrontal cortex, and activity in these regions predicted subsequent risk taking. Brain areas associated with cognitive control were less strongly recruited by adolescents than adults, but activity in the cognitive control system did not vary with social context. Results suggest that the presence of peers increases adolescent risk taking by heightening sensitivity to the potential reward value of risky decisions.
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              Biological substrates of emotional reactivity and regulation in adolescence during an emotional go-nogo task.

              Adolescence is a transition period from childhood to adulthood that is often characterized by emotional instability. This period is also a time of increased incidence of anxiety and depression, underscoring the importance of understanding biological substrates of behavioral and emotion regulation during adolescence. Developmental changes in the brain in concert with individual predispositions for anxiety might underlie the increased risk for poor outcomes reported during adolescence. We tested the hypothesis that difficulties in regulating behavior in emotional contexts in adolescents might be due to competition between heightened activity in subcortical emotional processing systems and immature top-down prefrontal systems. Individual differences in emotional reactivity might put some teens at greater risk during this sensitive transition in development. We examined the association between emotion regulation and frontoamygdala circuitry in 60 children, adolescents, and adults with an emotional go-nogo paradigm. We went beyond examining the magnitude of neural activity and focused on neural adaptation within this circuitry across time with functional magnetic resonance imaging. Adolescents showed exaggerated amygdala activity relative to children and adults. This age-related difference decreased with repeated exposures to the stimuli, and individual differences in self-ratings of anxiety predicted the extent of adaptation or habituation in amygdala. Individuals with higher trait anxiety showed less habituation over repeated exposures. This failure to habituate was associated with less functional connectivity between ventral prefrontal cortex and amygdala. These findings suggest that exaggerated emotional reactivity during adolescence might increase the need for top-down control and put individuals with less control at greater risk for poor outcomes.

                Author and article information

                Dev Cogn Neurosci
                Dev Cogn Neurosci
                Developmental Cognitive Neuroscience
                28 February 2015
                June 2015
                28 February 2015
                : 13
                : 11-20
                [a ]Department of Experimental Psychology, University of Oxford, Oxford, UK
                [b ]Department of Psychology, Institute of Psychiatry, King's College London, London, UK
                Author notes
                [* ]Corresponding author at: Department of Experimental Psychology, University of Oxford, Tinbergen Building, 9 South Parks Road, OX1 3UD Oxford, UK. Tel.: +44 (0) 1865-271382 simone.haller@ 123456psy.ox.ac.auk
                © 2015 The Authors

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).


                social anxiety,sad,cognitive bias,neurocognitive development,fmri,adolescence
                social anxiety, sad, cognitive bias, neurocognitive development, fmri, adolescence


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