Cognitive Models Of Social Anxiety Disorder Research Articles

Reduced early neural processing of faces in children and adolescents with social anxiety disorder

Social anxiety disorder (SAD) is one of the most common mental disorders during childhood and adolescence. Yet, little is known about its maintenance in youth. Cognitive models of SAD indicate that attentional biases play a key role in the dysfunctional processing of social information, such as emotional faces. However, previous research investigating neural correlates of childhood SAD has produced inconsistent findings. The current study aims to investigate neural face processing in children and adolescents with SAD, while taking into consideration methodological limitations of previous studies. We measured event-related potentials (P100, N170, EPN, LPP) in response to happy, neutral, and angry adult faces, and non-social household objects, in a sample of youth (aged 10–15 years) with SAD (n = 57), clinical controls with specific phobias (SP; n = 41), and healthy controls (HC; n = 61). Participants completed an emotion/object identification task while continuous EEG was recorded. Analyses revealed lower N170 amplitudes in the SAD group compared to HCs, irrespective of emotion. In addition, younger children (aged 10–12 years) with SAD showed lower EPN amplitudes and higher early LPP amplitudes (only trend level) in response to neutral and happy faces compared to younger HCs. These effects were specific to faces and were not evident in the neural processing of non-social household objects. Overall, the findings indicate that different neural response patterns are already present in youth with SAD. Group differences, particularly in younger children, suggest age-related differences in neural face processing in childhood SAD and underpin the necessity of developmental approaches.

Cognitive Factors in Social Anxiety Disorder and Relevant Interventions

Understanding how social interactions and fear responses affect mental health requires research on cognitive aspects of social anxiety disorder (SAD). SAD could be a substantial factor in a person's emotional, interpersonal, and professional areas of life. By examining cognitive issues, researchers can develop more effective treatments by understanding the biases and thought patterns that can contribute to the emergence and duration of SAD. Previous research focused on cognitive functioning, self-esteem, attentional biases, and the impact of cognitive biases on social interactions. The information-processing model and the cognitive model of SAD, which emphasizes negative interpretations and high expectations of oneself, are the main theories. To improve therapeutic outcomes, studies primarily focused on people with social anxiety across a range of age groups. In looking at different studies done on interventions for SAD, it has been shown that individualized treatment plans had the greatest impact on diminishing SAD symptoms and treating individuals to overcome their anxiety.

“Being Unfilial Condemns You to Hell”: Integrative Treatment for Social Anxiety Shaped by Domestic Abuse, Confucian Values, and Taoist Beliefs

Social anxiety is a common and treatable condition but less is known about how to adapt evidence-based approaches in a culture-sensitive way to Asian clients. We present the case of “Sally,” a 25-year-old Chinese Singaporean female who suffered from severe and long-standing social anxiety disorder (SAD), and secondary low mood. Contributing factors included a history of domestic abuse, as well as culturally influenced authoritarian parenting emphasizing the Confucian value of filial piety and reinforced by Taoist beliefs of karmic retribution and supernatural punishment. Treatment was based on Clark and Wells’s cognitive model of SAD with a focus on behavioral experiments, and was enhanced using a schema mode formulation and imagery rescripting to address relevant early memories that were at the origin of the social anxiety. Sally received a total of 42 sessions over the course of 21 weeks, during which she made steady progress toward recovery. Her self-reported depression and social phobia fell from the “severe clinical” range pretreatment to the “non-clinical” range posttreatment; these gains were maintained at 6 months follow-up. Sally’s functioning fully recovered, and she returned to work and school. While behavioral experiments for dropping safety behaviors were useful for overcoming the social anxiety, schema formulation was important for providing Sally with insight to her thought process, and imagery rescripting was crucial for weakening her self-criticism and internalized black and white thinking on filial piety. The significance of culture and religion in SAD, and the potential of adapting cognitive therapy in a culture-sensitive way is discussed.

Processes and pathways mediating the experience of social anxiety and negative rumination

Negative rumination in social anxiety disorder (SAD) occurs in anticipation of a social event (pre-event rumination) and in its aftermath (post-event rumination). Both are proposed to be key maintaining factors of the vicious cycle of social anxiety. Despite this, there is a dearth of research investigating the processes that mediate the relationship between social anxiety and pre-event rumination and uncertainty regarding the cognitive and attentional processes that mediate the relationship between social anxiety and post-event rumination. To investigate this further, the current study utilised a clinical sample of participants with SAD to determine the hypothesised mediators of a social anxiety and pre-event model (N = 239) and a social anxiety and post-event rumination model (N = 216). Results from path analyses were broadly consistent with cognitive models of SAD that posit several interrelated processes mediate the relationship between social anxiety and pre- and post-event rumination. Results also indicated slightly different processes showed stronger prediction of pre-event rumination (i.e., biased performance appraisals) and post-event rumination (i.e., negative attentional focus). Treatment recommendations that aim to address the maladaptive role of negative rumination in social anxiety are made in keeping with the inter-connected and dynamic role played by cognitive and attentional processes in heightening social anxiety.

On the context dependency of implicit self-esteem in social anxiety disorder

Background and objectivesCognitive models assume that negative self-evaluations are automatically activated in individuals with Social Anxiety Disorder (SAD) during social situations, increasing their individual level of anxiety. This study examined automatic self-evaluations (i.e., implicit self-esteem) and state anxiety in a group of individuals with SAD (n = 45) and a non-clinical comparison group (NC; n = 46). MethodsParticipants were randomly assigned to either a speech condition with social threat induction (giving an impromptu speech) or to a no-speech condition without social threat induction. We measured implicit self-esteem with an Implicit Association Test (IAT). ResultsImplicit self-esteem differed significantly between SAD and NC groups under the speech condition but not under the no-speech condition. The SAD group showed lower implicit self-esteem than the NC group under the speech-condition. State anxiety was significantly higher under the speech condition than under the no-speech condition in the SAD group but not in the NC group. Mediation analyses supported the idea that for the SAD group, the effect of experimental condition on state anxiety was mediated by implicit self-esteem. LimitationsThe causal relation between implicit self-esteem and state anxiety could not be determined. ConclusionThe findings corroborate hypotheses derived from cognitive models of SAD: Automatic self-evaluations were negatively biased in individuals with SAD facing social threat and showed an inverse relationship to levels of state anxiety. However, automatic self-evaluations in individuals with SAD can be unbiased (similar to NC) in situations without social threat.

Anticipatory Processing, Maladaptive Attentional Focus, and Postevent Processing for Interactional and Performance Situations: Treatment Response and Relationships With Symptom Change for Individuals With Social Anxiety Disorder

Anticipatory processing, maladaptive attentional focus, and postevent processing are key cognitive constructs implicated in the maintenance of social anxiety disorder (SAD). The current study examined how treatment for SAD concurrently affects these three cognitive maintaining processes and how these processes are associated with each other as well as with symptom change from pre- to posttreatment. The sample consisted of 116 participants with SAD receiving group cognitive behavioral therapy. All three cognitive maintaining processes were measured relative to a speech task and again relative to a conversation task. Across both tasks, the three cognitive process variables demonstrated decreases from pre- to posttreatment. Within the same task, a slower rate of decrease in a specific cognitive process variable from pre- to posttreatment was predicted from higher pretreatment levels of either one or both of the other cognitive process variables. Additionally, higher levels of pretreatment conversation-related anticipatory processing and maladaptive attentional focus predicted a slower rate of decrease in social anxiety symptoms from pre- to posttreatment. Results are consistent with cognitive models of SAD and have important implications for enhancing existing treatments.

Negative rumination in social anxiety: A randomised trial investigating the effects of a brief intervention on cognitive processes before, during and after a social situation

Background and objectivesAccording to cognitive models of Social Anxiety Disorder (SAD), negative rumination is a key maintaining factor in the vicious cycle of social anxiety. However, there is a scarcity of research investigating treatment effects on rumination in social anxiety, as well as other key cognitive variables. The current study aimed to determine the effectiveness of a brief intervention on a range of cognitive processes, most notably negative rumination. Additionally, predictors of negative rumination and state anxiety are also investigated. MethodsParticipants with a diagnosis of SAD were randomly allocated to an intervention (n = 24) or control group (n = 23). Participant's initially completed trait and state based measures with the intervention group also completing a brief cognitive intervention. One-week later participants completed state anxiety and cognitive measures before and after a speech task. Finally, one-week post-speech task participants completed further trait and state based measures. ResultsWhile the brief cognitive intervention had positive effects on some of the cognitive processes measured at different time points of the study, levels of negative rumination remained stable. Predictors of negative rumination and state anxiety were consistent with cognitive models of SAD. LimitationsThe brief nature of the intervention and temporal stance of the intervention (delivered one-week before the speech) may have impacted outcomes. ConclusionsCognitive technique can potentially impact a range of key processes that maintain SAD, however, more powerful and tailored interventions are needed that address the different processes at play before, during and after a social situation for socially anxious individuals.

Area-dependent time courses of brain activation during video-induced symptom provocation in social anxiety disorder.

BackgroundPrevious functional imaging studies using symptom provocation in patients with social anxiety disorder (SAD) reported inconsistent findings, which might be at least partially related to different time-dependent activation profiles in different brain areas. In the present functional magnetic resonance imaging study, we used a novel video-based symptom provocation design in order to investigate the magnitude and time course of activation in different brain areas in 20 SAD patients and 20 healthy controls.ResultsThe disorder-related videos induced increased anxiety in patients with SAD as compared to healthy controls. Analyses of brain activation to disorder-related versus neutral video clips revealed amygdala activation during the first but not during the second half of the clips in patients as compared to controls. In contrast, the activation in the insula showed a reversed pattern with increased activation during the second but not during the first half of the video clips. Furthermore, a cluster in the anterior dorsal anterior cingulate cortex showed a sustained response for the entire duration of the videos.ConclusionsThe present findings suggest that different regions of the fear network show differential temporal response patterns during video-induced symptom provocation in SAD. While the amygdala is involved during initial threat processing, the insula seems to be more involved during subsequent anxiety responses. In accordance with cognitive models of SAD, a medial prefrontal region engaged in emotional-cognitive interactions is generally hyperactivated.

Social performance deficits in social anxiety disorder: Reality during conversation and biased perception during speech

Cognitive models emphasize that patients with social anxiety disorder (SAD) are mainly characterized by biased perception of their social performance. In addition, there is a growing body of evidence showing that SAD patients suffer from actual deficits in social interaction. To unravel what characterizes SAD patients the most, underestimation of social performance (defined as the discrepancy between self-perceived and observer-perceived social performance), or actual (observer-perceived) social performance, 48 patients with SAD and 27 normal control participants were observed during a speech and conversation. Consistent with the cognitive model of SAD, patients with SAD underestimated their social performance relative to control participants during the two interactions, but primarily during the speech. Actual social performance deficits were clearly apparent in the conversation but not in the speech. In conclusion, interactions that pull for more interpersonal skills, like a conversation, elicit more actual social performance deficits whereas, situations with a performance character, like a speech, bring about more cognitive distortions in patients with SAD.

The Neural Correlates of Social Anxiety Disorder and Response to Pharmacotherapy

This study attempted to define further the neural processing events underlying social anxiety in patients with social anxiety disorder (SAD) and their response to pharmacotherapy. Social anxiety-related changes in regional cerebral blood flow were defined by [15O]H2 positron emission tomography (PET) in medication-free individuals with generalized SAD (gSAD), and age- and sex-matched comparison subjects, and analyzed using a linear mixed effects model. PET studies were again acquired in the gSAD individuals following an 8-week, flexible dose treatment trial of nefazodone. Both script-guided mental imagery of an anxiogenic social situation and a confrontational mental arithmetic task were associated with marked increases in self-rated anxiety in both subject groups. For gSAD subjects, social anxiety induced by guided mental imagery was associated with increased activity in the left postcentral gyrus and lenticulate, and the right inferior frontal and middle temporal gyri. Social anxiety induced by the mental arithmetic task was associated with activation of the medial and left dorsolateral prefrontal cortex, cerebellum, thalamus, insula, and ventral striatum. Both tasks were associated with relative decreases in activity in the right amygdala and the hippocampus. A direct group comparison indicated that comparison subjects exhibited a differing pattern of social anxiety-related neural activations. Nefazodone treatment was associated with marked clinical improvement. Comparison of social anxiety-related neural activations prior to and after nefazodone administration indicated greater activity in the precentral gyrus, insula, midbrain/hypothalamus, and middle frontal and anterior cingulate gyrus prior to treatment, and greater activity in the left middle occipital and bilateral lingual gyri, postcentral gyrus, gyrus rectus, and hippocampus after treatment. The results of an analysis relating neural activity and treatment-related changes in symptom severity indicated differential neural responses associated with states of symptom remission vs partial response. The observed social anxiety-related changes in distributed neural activity are consistent with cognitive models of SAD and adaptive decreases in amygdala activity in response to social anxiogenics, and support the association of altered frontal cortical responses with treatment response.