Social Anxiety Disorder Introductory Chapters PDF
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This document provides an introduction to social anxiety disorder, covering its defining characteristics, prevalence rates, potential causes, including genetic and developmental factors, and the cognitive processes involved in the disorder. The document also offers insights into the treatment approaches for this condition.
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Task 3 - Not a fan of PBL Introductory chapters on social anxiety disorder Definition Social anxiety disorder - a severe & persistent fear of social or performance situations. The anxiety of social situations is so pervasive that it predicts comorbiditi...
Task 3 - Not a fan of PBL Introductory chapters on social anxiety disorder Definition Social anxiety disorder - a severe & persistent fear of social or performance situations. The anxiety of social situations is so pervasive that it predicts comorbidities (e.g. with other mood & anxiety disorders & substance abuse). Individuals with the disorder sometimes are anxious that they will show anxiety symptoms that will be negatively evaluated by others (e.g. they will be humiliated or rejected or offend others). They may avoid eating/drinking in public due to fear that others will see their hands shake. They almost always experience anxiety symptoms (e.g. palpitations, sweating, gastrointestinal discomfort, diarrhea, muscle tension, blushing, confusion) in the fear social situations. In severe cases, these symptoms may develop into panic attacks. People with SAD engage in safety behaviors, which aim to reduce their anxiety (e.g. avoiding eye contact or avoidance of soci al situations altogether). Individuals with the disorder tend to underperform at work & school, have impaired social & romantic relationships and lower productivity as a result of their avoidance of social situations, they have lower life satisfaction, and higher suicidal ideation and risk for depression. Prevalence Lifetime prevalence is 4-13% in Western societies. Gender prevalence is 3:2 females to males Women with the disorder tend to have more severe social fears than men, particularly in performance -related situations (e.g. giving a presentation), whereas men tend to seek treatment more often, possibly because their fears often include dating situations. Age of onset is earlier than many other anxiety disorders, with a typical age of onset being early -middle teens, usually before 18 years of age. Onset of new cases beyond late adolescence are uncommon and often secondary to another mental disorder. It is a particularly persistent disorder, and has the lowest remission rate of the main anxiety disorders. Prevalence estimates are lower for East Asian countries, but this may be due to different expression of social anxiety in tho se countries. In Western societies social anxiety mostly revolves around embarrassing oneself, while in e.g. Japan it may be more connected to offending others. Social anxiety disorder is chronic if left untreated, and most people do not seek treatment. The etiology of social anxiety disorder Although it is a phobia, social anxiety disorder is classified separately from specific phobias partly due to the unique cogn itive biases its sufferers have. Genetic factors Twin studies suggest that there is significant but moderate genetic influence on development of social anxiety disorder. Specific constructs that are related to the disorder and are heritable are submissiveness, anxiousness, social avoidance and behavioral inhibition (a construct used to define characteristics of some children who seem quiet, isolated and anxious when confronted with social situations o r novelty). Other studies have indicated that there is a general predisposition to anxiety disorders that is inherited, rather than socia l phobia specifically. Heritable characteristics specific to social anxiety disorder have been estimated to account for 13% of the variance in social fear, while the estimate for general anxiety characteristics is 30-50%. Familial and developmental factors Offspring with social anxiety disorder are more likely to have parents (especially mothers) with social anxiety disorder. There is considerable evidence that children with a behaviorally inhibited (BI) temperament style have a higher risk for deve loping the disorder. BI has a heritability of 50-70% and is considered a risk factor for developing the disorder. However, many BI children do not develop it => it is not a sufficient condition. Early parent-child interaction styles may also play a role in the development of social anxiety disorder. Parents of children with social anxiety disorder are more controlling, show less warmth, are less sociable, and also use shame as a method of discipline. However, it is unknown if these factors are causal. Over 90% of people with SAD report humiliating experiences early in their lives that contributed do their symptoms (e.g. extr eme teasing as a child). Cognitive factors People with SAD have an information processing & interpretation bias in which they make excessively negative predictions abou t future social events. Individuals with SAD rate the probability of negative social events occurring as higher than people with other anxiety disorders and controls. This negative evaluation is likely to maintain their avoidance of social situations. They tend to notice potentially threatening social cues (e.g. grimace on other people's faces) & misinterpret them in self-defeating ways. People with SAD interpret their performance in social situation significantly more critically than non-sufferers and independent observers. They also underestimate their social skills and find it hard to process positive social feedback. Study: high and low socially anxious participants were asked to give a speech to a group of observers. After giving the speech, the high socially anxious participants rated the observers’ enjoyment of their speech significantly lower than low socially anxious participants. The high socially anxious participants even do this when the observers have been instructed to provide positive feedback, suggesting that socially phobic individuals do not attend to positive feedback cues given by an audience. This focus on negative aspects of social situations, and the inability to take anything 'good' from a social performance are likely to maintain one's dysfunctional beliefs that social situations are threatening and that their own performance is likely to be flawed. People with SAD have unrealistically high standards about their social performance (e.g. thinking that everyone needs to like them). Psychopathology Page 1 People with SAD have unrealistically high standards about their social performance (e.g. thinking that everyone needs to like them). Self-focused attention - SAD sufferers show a strong tendency to shift their attention inwards onto themselves and their own anxiety responses during social performance - especially when they fear they will be negatively evaluated. This makes socially anxious people believe that they look as anxious as they feel inside. This prevents them from objectively processing the situation, engage in critical self-evaluation, and may negatively affect their performance. Socially anxious people self-report self-focused attention more, and tend to recall social memories more often from an observer (than a personal) perspective. Socially anxious people also engage in excessive post-event processing of social events, during which they critically evaluate themselves and their performance. Such post-event rumination maintains negative appraisals, social anxiety, and avoidance. Treatment of social anxiety disorder Both pharmacological treatments and CBT are used for the treatment of SAD and are effective. Successful CBT treatments include the following elements: Exposure therapy - the client stays in a feared social situation despite distress - either in vivo or through role playing with the therapist. Exposure starts with the least anxiety-provoking situations and progresses to the most anxiety-provoking ones. Social skills training - addresses the social skills deficits that social phobics have, through modelling, behavioral rehearsal, corrective feedback & positive reinforcement. Cognitive restructuring - challenges & replaces the cognitive biases & reduces self-focused attention. Monoamine-oxidase inhibitors, SSRIs benzodiazepines & beta-adrenergic blockers cause improvements in social anxiety symptoms. However, drug therapy & CBT have complementary benefits: drugs have a faster effect, but CBT is required to maintain the gains over time. If only drugs are used, symptoms tend to return after their usage is stopped. Mindfulness-based interventions are also effective for social anxiety disorder. They teach individuals to be less judgmental about their own thoughts and reactions, and to be more focused on & relaxed in the present moment. Therapies such as acceptance & commitment therapy (ACT), which builds on CBT to emphasize mindfulness, acceptance and values, are similar to CBT in effectiveness for SAD. CBT group therapies are equally effective for SAD. Group settings allow a natural way to engage patients in social situations, increasing exposure while also building social skills. Nolen-Hoeksema - Agoraphobia & Panic disorder Agoraphobia Agoraphobia - a disorder where people fear places where they may have trouble escaping or getting help if they are anxious (e.g. in public transport, open spaces, in shops, in crowded places, or anywhere alone outside their home). 50% of people with agoraphobia have a history of panic attacks that precede the development of agoraphobia. The rest typically have a history of another anxiety disorder, a somatic symptoms disorder or depression. Agoraphobia most often begins during early 20s and is more common in women than men. People with agoraphobia often reach the point where they will not leave their homes alone. When they try to force themselves into frightening situations, they experience persistent & intense anxiety, causing them to retreat to their homes. Some abuse substances to dampen their anxiety symptoms. Panic disorder 28% of adults have occasional panic attacks, especially during stressful times. However, for most, the attacks are isolated e vents that do not change how they live their lives. A panic disorder diagnosis is made if the panic attacks become common, when they are not provoked by any particular situation, but are unexpected, when a person begins to worry about having them, and changes behaviors as a result of this worry. People with panic disorder often fear that they have a life-threatening illness, and they are more likely to have a personal/family history of serious chronic illness. After such an illness is ruled out, they may continue to believe that they are about to die of a heart attack, seizure etc. They also often think that they are "going crazy" or "losing control." If left untreated, people with panic disorder may become demoralized and depressed. Prevalence Lifetime prevalence of panic disorder is 3-5%. Typical age of onset is between late adolescence and mid-30s. It is more common in women and tends to be chronic. Comorbidities include generalized anxiety, depression, and alcohol abuse. Comorbid PD with substance abuse or depression is especially associated with suicide attempt risk. Theories of panic disorder Many people with panic disorder have a biological vulnerability to it. Heritability of panic disorder is about 43-48%. No specific genes have been identified. Psychopathology Page 2 Heritability of panic disorder is about 43-48%. No specific genes have been identified. The fight-or-flight response is poorly regulated in people who develop the disorder. People with PD have dysregulation of norepinephrine systems in the locus ceruleus, which has pathways to the limbic system. It is possible that poor regulation in the locus ceruleus may cause panic attacks, which then stimulate the limbic system, lowering the threshold for the activation of diffuse & chronic anxiety. Then the anticipatory anxiety may increase the likelihood of dysregulation of the locus ceruleus and thus of another panic attack. Psychological factors also determine who develops the disorder. People prone to panic attacks tend to pay very close attentio n to their bodily sensations, misinterpret these sensations in a negative way, and engage in catastrophic thinking, exaggerating symptoms & their consequen ces (in detail in the articles below). Interoceptive conditioning - the association between bodily cues (CS) and anxiety/panic attacks. People prone to panic attacks appear to have increased interoceptive awareness. Through interoceptive conditioning, slight increases in anxiety (even unconscious ones) can elicit conditioned fear that grows into a full panic attack. If the person does not recognize this process, the panic attack appears to come out of nowhere. An integrated model of biological & psychological factors has been developed: Treatment of panic disorder Drug therapies include SSRIs, SNRIs, and benzodiazepines. Most people with PD experience a relapse of symptoms when drug treatment stops if they have not received CBT. CBT interventions for PD include the following components: Relaxation & breathing exercises, which give patients control over their symptoms and allow them to engage in other components of the therapy. Identifying & challenging catastrophizing cognitions (e.g. with a thought diary). Some patients find it difficult to pay attention to their thoughts during a panic attack, which is why the therapist may induce symptoms during sessions (e.g. by having clients exercise to elevate their heart rate, spin to get dizzy etc.) and help patients collect their thoughts. Using systematic desensitization to expose client gradually to feared situations while helping them maintain control over their symptoms. CBT is considerably better than antidepressants at preventing relapse after treatment ends. Cognitive mediation of panic attacks induced by biological challenge tests - Clark Article (1993) Introduction A variety of pharmacological and physiological procedures can reliably induce panic attacks in panic disorder patients, but r arely do so in normal controls, or in patients with other anxiety disorders. Such procedures include infusions of sodium lactate and cholecystokinin-tetrapeptide, oral administration of yohimbine, prolonged inhalation of 5% CO2, single-breath inhalations of 35%-50% CO2 and voluntary hyperventilation. These procedures have been described as biological challenge tests, under the assumptions that they induce panic directly and that individuals who are susceptible have a neurochemical disorder. An alternative explanation is that panic attacks are a result of the misinterpretation of benign bodily sensations as indicat ions of impending physical or mental catastrophe. Criteria for establishing cognitive mediation To demonstrate that panic attacks induced by biological challenge tests are cognitively mediated requires to show that: Panic disorder patients have a stronger tendency to misinterpret certain bodily sensations than controls. Thoughts based on the misinterpretation of bodily sensations accompany challenge-induced panic attacks. Experimental manipulations of cognitive variables have an influence on whether or not someone panics during a biological challenge test. Criterion 1 Study: panic disorder patients were more likely to interpret bodily sensations as signs of an impending physical or mental di sorder than other anxiety disorder patients or normal controls. Several other studies have also reviewed criterion 1. Psychopathology Page 3 Criterion 2 Study: panic attacks induced by single inhalations of 50% CO, are accompanied by catastrophic cognitions such as “I am going to die”. Similar results have been found when using the 5% CO 2-induced panic attacks. Criterion 3 Study: a pre-challenge instruction was used to manipulate patients' interpretation of the sensation induced by a single inhalation of 50% CO2. 1/2 of the panic disorder patients were allocated to a no explanation condition in which minimal information about the procedure was provided. The other 1/2 were given a more detailed explanation in which all possible sensations were described and attributed to the effects of the gas. A manipulation check confirmed that the detailed explanation group had less catastrophic cognitions during the inhalation. The explanation group also reported significantly less panic than the no explanation group. Social phobics who were subjected to the same manipulation reported low panic ratings in both conditions => the panic-inducing effect of 50% CO2 is specific to panic disorder patients. A problem of this study (addressed in the next) is that the explanation group may have held their breath for a shorter time because they knew what the effects of the gas would be. Study: a deception was used to manipulate patients' perceived control during a 20-min inhalation of 5% CO2 enriched air. Before the start of the inhalation, panic disorder patients are shown a dial and told that turning it would reduce CO2 flow if a nearby light was illuminated but not otherwise (in fact it had no effect on CO2). During the infusion the light came on for half the patients (illusion of control group) but not for the rest (no illusion of control group). The illusion of control ground tended to report less catastrophic cognitions than the no illusion group, and were significantly less likely to panic (20% vs. 80% even though they received as much CO2 as the no illusion group). Study: prior to 3 minutes of strenuous hyperventilation (60 breaths/minute) panic patients' expectations were manipulated by describing the hyperventilation procedure either as a "fast-paced breathing task" or as a "biological panic attack test." A manipulation check confirmed higher distress expectations for the latter group. Patients in the latter group rated the effects of hyperventilation as significantly more similar to their naturally occurring panic attacks and reported significantly more panic symptoms than the other patients. Study: panic disorder patients are allocated to 1 of 2 instructions before infusion of sodium lactate. Both sets of instruction emphasized that lactate is natural & harmless and the infusion could be stopped at any time, and that it is normal to experience sensations, and that they do not indicate an adverse bodily reaction. The experimental group were encouraged to ask questions and give answers supporting the view that strong sensations are a normal consequence of the infusion. The control group wasn't. Manipulation check confirmed that the experimental group were more likely to believe the experienced sensations are normal. Patients in the experimental group reported less anxiety, had smaller heart rate increases and were less likely to panic. Is the panic response to all biological challenge tests cognitively mediated Panic disorder patients appear to be better than controls are detecting bodily processes, such as cardiac changes (they have higher interoceptive awareness). Study: yohimbine and CCK produce in panic patients discernible sensations before the onset of attacks, but not in normal controls. Once noticed, these sensations could then be misinterpreted => there is reason to believe that cognitive mediation also exists for other biological challenge tests. Is there a critical cognitive mediator? 3 different cognitive variables were shown to be a mediator of biological challenge producing a panic response: Expected affect - subjects' expectation about the distress and anxiety they might experience during the procedure. Interpretation - the explanations that were readily available for sensations experienced during the procedure. Perceived control - subjects' perceived control over the sensations that may be experienced during the procedure. The authors propose that the crucial cognitive variable is likely to be the interpretation of challenge -induced sensations, rather than expected affect or perceived control of the sensations. Manipulations of perceived control will almost inevitably influence the interpretations that are available to a subject. It's also difficult to see how reducing perceived control could reduce fear without reducing the perceived danger of the feared stimulus. Catastrophic cognitions in panic disorder with and without agoraphobia - Khawaja Article (1998) Cognitive models of panic disorder (PD) and panic disorder with agoraphobia (PDA) emphasize the concepts of catastrophic misinterpretation and catastrophic cognitions. Catastrophic misinterpretation - autonomic arousal is misinterpreted as more dangerous than it is. Catastrophic cognitions - cognitions with themes of danger, disaster or threat are experienced by patients as a result of catastrophic misinterpretation. These models state that bodily sensations (mainly those involved in a normal anxiety response, e.g. palpitations, breathlessness & dizziness) are produced by internal/external cues. Panic-prone individuals are sensitive & hypervigilant to these bodily sensations. They tend to focus their attention on them and when they are unable to interpret the sensations in a realistic manner, they misinterpret them as being dangerous and potentially leading to a disaster. This misinterpretation can occur so quickly & automatically that the individual may not be aware of it. Therefore, in PD and PDA panic does not result from strong physical sensations but from the belief that these sensations are dangerous. Agoraphobic patients are afraid of specific situations (e.g. elevators) and they may experience a panic in places where they experienced panic before. On entering a feared place, an agoraphobic tends to become anxious in anticipation of a further attack and selectively focuses on the body, noticing unpleasant sensations. These sensations are misinterpreted as dangerous and as indicating a coming attack. They activate a vicious cycle that actually produces a panic attack, which then leads to the agoraphobic fears and avoidance of the situation. This article reviews the literature to evaluation the empirical support for cognitive models of PD/PDA. Catastrophic misinterpretations Psychopathology Page 4 Panic induction and cognitive features The previous article's studies are discussed as evidence for catastrophic misinterpretations and for the fact that cognitions play a role in the development & maintenance of panic disorder. Panic induction by cognitive manipulation Study: PD patients, recovered PD patients and normal controls read aloud a series of paired associates linking bodily sensati ons and catastrophes (e.g. palpitations-dying). 83% of PD patients experienced a panic attack, yet no attacks were experienced by the recovered patients or the normal controls. Study: claustrophobic students stay in a small chamber for 3-5 minutes. Before entering the chamber, they read a list of the DSM-III panic attack symptoms. While in the chamber, 1/2 are asked to concentrate on their body, while the rest are asked to concentrate on a neutral object. Participants who concentrated on their body reported higher panic scores and more misinterpretations of bodily symptoms. Study: PD patients, PDA patients and normal controls told that their heart rate experienced abruptly (it actually didn't). The patients rated their anxiety & excitement higher, and they had higher heart rate, SCR, and blood pressure after the false feedback. In another study, a similar heart rate procedure induced a full-blown panic attack in a PD patient. Interpretation of ambiguous stimuli Catastrophic misinterpretation should be most likely when the cause of the bodily sensation is ambiguous and least likely whe n there is a benign explanation for the sensation. Study: both internal & external stimuli were interpreted as more threatening by untreated agoraphobics as compared with treated agoraphobics and healthy controls. Study: PD patients, compared to patients with order anxiety disorders, are more likely to misinterpret bodily sensations in a negative fashion. This does not apply to other ambiguities => PD patients do not misinterpret ambiguity in general, but ambiguity related to bodily sensations. Even recovered agoraphobics misinterpret ambiguous information within the context of bodily sensations as threatening. Information processing studies PD/PDA patients exhibit attentional biases for processing disorder-specific threat information. They are hypervigilant and scan for external & internal cues related to their disorder. Once the threatening cues become the focus of attention, patients tend to misinterpret them as more dangerous than they really are. This attentional bias is not specifically related to anxiety or panic cues, but may reflect a more generalized trend of focusing on emotional cues. In the Stroop task, patients with GAD tend to process threat cues selectively, even when they are instructed to ignore them. There is a clear relationship with the type of worry (social/physical) and the word that produces interference. PD/PDA patients also exhibit memory biases - due to the attentional biases & follow-up elaboration of negative events, these events are more accessible in memory and more likely to contribute to anxiety. Study: nonclinical panickers recall more anxiety words than neutral words and more danger than hostility words in a free recall task, compared to nonpanickers. Study: PD patients showed better perceptual & semantic memory for threat words as compared to positive and neutral words. Normal controls showed no effect of stimulus type. Therefore, PD patients engage in preferential processing of threat information at both perceptual and semantic levels of analysis. Catastrophic cognitions Interview studies PD/PDA patients engage in frequent thoughts of dramatic consequences. Study: PD patients report thoughts concerned either with anticipated physical catastrophes (death, heart attack, fainting, loss of breath, illness & seizure), mental catastrophes (going crazy), and behavioral catastrophes (loss of control) during a panic attack. Some (around 40%) feared social humiliation as a result of physical & mental catastrophes. Interview studies assessed cognitions during panic retrospectively => the results may be affected by recall biases. Questionnaire studies Catastrophic Cognitions Questionnaire (CCQ) - a questionnaire with 3 factors that was developed to measure catastrophic cognitions. Emotional catastrophes - the misinterpretation of affective responses (e.g. feeling jittery, shaky, angry or uncomfortable are typical unpleasant experiences typical of anxiety) as dangerous. Physical catastrophes - anxious and panic-prone individuals are sensitive to somatic sensations - those are exaggerated and interpreted as an indication of stroke serious injury, or passing out. Mental catastrophes - strained cognitive capacity is considered as dangerous, indicating a possibility of mental derangement. An anxious person's tendency to focus on and monitor his internal emotional & somatic reactions can result in the inhibition of many normal functions. One's capacity may be so taxed by coping with perceptions of danger that little capacity is left to satisfy other demands of cognitive processing. Thinking difficulties may include mental blocking, interference in recall, and faulty reasoning. The CCQ has good psychometric properties and the 3 factor structure was confirmed on both non-clinical and anxiety disorder patients. Self-monitoring studies Study: PD patients record their cognitions during an attack using a panic diary. 79% of panic attacks were associated with 1 or more types of fearful cognition (mental, physical or social) and all patients experienced >=1 panic attack associated with cognitions of danger. Study: 36 PD patients recorded 285 panic attacks over a 2-week period. 91% of panic attacks (>=4 symptoms) contained catastrophic cognitions, whereas only 57% of the limited-symptom attacks ( people with SAD are biased towards a negative perception of their own performance. Performance appraisals are the most unique predictor of post-event rumination within clinical samples of SAD. Study: participants complete a 3-minute speech task immediately followed by a subjective measure of public speaking performance, as well as a post- event rumination questionnaire 1 week later. Individuals' performance appraisals in a speech task completely mediated the association between social anxiety levels and the amount of post- event rumination. This relationship may be bidirectional: cognitive biases related to performance perception lead to negative rumination, which in turn leads to an augmentation of the negative representation of their performance in long-term memory. Threat appraisals (overestimation of probability & consequences of a feared social outcome) play a significant role in mainte nance of SAD & mediate treatment outcome. They also predict increased post-event rumination. The findings about whether fear of negative evaluation, self-imagery & self-efficacy, and self-focused attention are unique predictors of negative rumination in SAD are mixed or insufficient. Pre-event rumination Pre-event rumination in SAD has more overlap with worry than post-event rumination, because it is future-oriented (e.g. What if I embarrass myself at the party?). However, it is still distinct from worry due to preoccupation with memories of past social situations & the meaning of past perceived social failures (e.g. Why do I keep embarrassing myself at parties?). Individuals with SAD are more likely to engage in pre-event rumination before a social situation than healthy controls. The amount of post-event rumination is predicted by the standards (high or low) that they perceive for the social situation. Predictors of pre-event rumination Pre- and post-event rumination are sometimes theorized to be similar, but there is some evidence that they have different predictors. Study: pre-event rumination variance was explained by anticipated self-appraisals of performance, threat appraisal, self-efficacy & state anxiety. Post- event rumination variance was explained only by threat appraisals. Role of rumination in mediating treatment effects for SAD Greater levels of post-event rumination are related to poorer treatment outcomes of SAD; reductions in post-event rumination are associated with reduced SAD symptoms. Cognitive restructuring and mindfulness treatments can reduce post-event rumination for SAD. There are no studies on pre-event rumination. Therapeutic strategies for social anxiety disorder: where are we now? - Pelissolo Article (2019) Introduction Performance only SAD - SAD with fears related to public speaking or speaking up in a meeting/class. Generalized SAD - SAD where the patient is anxious in many social situations in which they are the center of attention and fear to be criticize d. Psychological treatment Classical CBT Classical CBT is based on the Clark & Wells model or the Heimberg model and consists of 15 sessions of 60 - 90 minutes each. Psychopathology Page 8 Classical CBT is based on the Clark & Wells model or the Heimberg model and consists of 15 sessions of 60 - 90 minutes each. It includes education about social anxiety, gradual exposure to feared social situations, experiential exercises to show the negative effects of self-focused attention & safety behaviors, emotion regulation, video feedback to correct distorted negative self-imagery, cognitive restructuring, and relapse prevention. More specific approaches have been developed (see table above - specific approaches). CBT effectiveness is supported by lots of research, and there is evidence that it is better than standard habituation -based exposure treatments. CBT gains have been shown to be maintained over a 2-year and a 10-year follow-up. Third-wave approaches to CBT CBT techniques were first based on behavioral (1st wave) then cognitive (2nd wave) techniques. In the 1990s, a 3rd wave of psychotherapies emerged, which consists of approaches aiming to change the way a patient relates to experienced distress, rather than changing the associated cognitions. 3rd wave interventions are based on psychological flexibility, values and acceptance. Many studies have confirmed the specific benefit of ACT & mindfulness-based stress reduction (MBSR) in the treatment of SAD. Internet-delivered psychotherapy Internet-delivered CBT (ICBT) has been developed to address the accessibility and lower the costs of CBT, overcoming barriers such as social inhibition, st igma and shame. ICBT consists of automated website & application-based programs, with no human interaction, or mixed programs that include both computerized sessions and sessions with a therapist). Comparative studies show that iCBT has comparable effectiveness to traditional CBT, good long-term outcomes and reduced costs. Virtual reality therapy Social exposure in VR can be used in CBT programs for people who are reluctant to engage in in vivo exposure exercises. There is evidence that CBT with VR exposure is just as effective as CBT with in vivo exposure. Attention bias modification Attention bias modification treatment (ABMT) has been developed to treat SAD via a reduction of attention biases towards socially threatening information and interpretational biases pushing individuals to view ambiguous events as threatening. It is a computer-based treatment and uses a version of the dot-probe task to implicitly teach the patient to systematically redirect attention away from socially threatening stimuli. Efficacy is controversial, due to mixed evidence. AMBT is not yet ready for wide-scale application as a treatment for SAD. Pharmacotherapy of social anxiety disorder Pharmacotherapy is considered first-line option for severe SAD, or an alternative strategy when CBT is ineffective, rejected by the patient, or when there is comorbid depression. SSRIs SSRIs are most researched in SAD and there is a lot of evidence that they work just as well as CBT (some studies have found w orse results than CBT). When effective, SSRIs not only reduce symptoms of SAD but also secondary disability and comorbid depression. SNRIs Selective norepinephrine reuptake inhibitors (SNRIs), specifically venlafaxine, is found to be more effective than placebo in treating SAD. Other antidepressants Phenelzine (a MAOI) is more effective than placebo but it is not recommended as first- or second-line treatment due to its adverse effects and dietary limitations. Moclobemide and brofaromine (other MAOIs) are modestly effective in SAD treatment, less than SSRIs, venlafaxine and phenelzin e. Benzodiazepines Benzodiazepines have short-term effects on SAD symptoms, but they are not suitable for a chronic disorder like SAD due to dependence & withdrawal symptoms associated with chronic use. Moreover, SAD patients cannot be cured with a benzodiazepine despite its short-term efficacy. Combined medication-psychological treatments Most guidelines recommend combination of drugs and psychotherapy for treating SAD, but there are relatively few trials showin g effectiveness of combined therapy compared to monotherapy. Impact of comorbidity SAD patients with comorbidity are more likely to have higher symptom severity, greater chronicity, decreased functioning, and higher rates of suicide. Comorbidity is also a risk factor for treatment resistance or poorer response to treatment. Treatment for children and young people with SAD SAD typically begins during childhood/adolescence and can significantly disrupt the children's quality of life, school perfor mance, peer relations, and social competence. Despite its negative impact, the majority of adolescents with SAD remain untreated, due to underdiagnosis and reluctance/difficulty of access to specific care. Meta-analyses have confirmed the efficacy of CBT in children and adolescents. A school-based CBT program was developed, that includes social skills training and behavioral exposures. This program has been shown to be effective for adolescents. Psychopathology Page 9 Psychotherapy is the first-line treatment for SAD in children/adolescents, but medication may be suggested for severe or non-responding cases. Expert opinion Most studies do not distinguish between performance-only and generalized SAD subtypes. However, pharmacotherapy, especially with SSRIs, is more effective for patients with the generalized subtype. Moreover, most patients with generalized SAD may require a longer duration of treatment and a combination of drugs & CBT to achieve significant improvement. Overall, available treatments are effective in 50-60% of cases. New treatments are needed for the non-responding 1/3 of cases. There is still not much evidence on treatment-resistant SAD. Social performance deficits in social anxiety disorder: Reality during conversation and biased perception during speech - Voncken Article (2008) Introduction Cognitive models emphasize that patients with SAD are mainly characterized by biased perception of their social performance. However, there is also a lot of evidence that SAD patients have actual deficits in social interaction. It may be useful to discriminate between speech & conversation tasks when investigating biased perception & actual performanc e deficits in social tasks. Conversation may require more complex interpersonal social behaviors than a speech (listening, asking questions, responding to what others say). A speech does not require interaction with the audience to such extent. Comparison with self- and observer ratings of performance have been used in many studies, but to assess cognitive discrepancies in SAD it is more p recise to compare self-ratings of how people believe observers will evaluate them with observers' actual evaluations. Study: social anxiety is characterized by a discrepancy between how patients perceive themselves and what they believe others want them to be. In contrast, depression is characterized by a discrepancy between how patients perceive themselves and how they ideally want to be. The current study investigates if patients with SAD are mostly characterized by biased perception or by actual performance de ficits in both speech & conversation. Method Generalized SAD patients and control participants have to give a speech in front of 2 confederates or get acquainted with the m. Biased perception was assessed by the discrepancy between confederates' social performance ratings and by participants' estimates of these ratings. Social Behavior and Anxious Appearance (SBA-rating scale) - a scale that has a 2-factor structure relating to anxious appearance (trembling, stuttering, appearing nervous) and social behavior (making eye contact & smiling). The SBA was completed by the 2 confederates (confederate rating), and 2 video-raters (video-rating), blind to the diagnoses of the participants. The participants rated their prediction of how the confederates would judge them (predicted rating). Results The inter-rater reliability on the SBA between the 2 confederates and between confederates and video raters was high. Confederates acted the same way toward the SAD and the non-clinical control group, as rated by video observers. SAD patients predicted to be rated worse by their confederates than the non-clinical controls on all measures: anxious appearance & social behavior during speech and conversation. The discrepancy between actual and predicted evaluation was higher for SAD patients compared to controls during the speech. During the conversation, discrepancy in social behavior ratings was insignificant (p=0.27) , and for anxious appearance only a borderline effect was found (p=0.06). The confederates rated SAD patients as showing a more anxious appearance and less adequate social behavior than the non -clinical controls during the conversation, but these differences were not significant during the speech. Since separating the SBA into the 2 factors did not help differentiate between the 2 groups, the following analyses were done by combining the 2 factors into a new variable "genera social performance." Conclusions mainly remained similar to those concerning the separated factors. However, during the conversation the underestimation of general social performance in the SAD group started to approach significance. Discussion Results revealed that patients with SAD, compared to a non-clinical control group: Underestimate their social performance primarily during a speech and to a lesser extent (only borderline significant) during a conversation. Show actual performance problems during a conversation but not during a speech. These conclusions were apparent in both anxious appearance and social behavior of the participants. This may be because: Speech requires mainly action, while conversations require interaction. Conversations are less structured, unpredictable and may be perceived as more uncontrollable. Conversations require more interpersonally sensitive social behavior than a speech: making contact, listening, showing interest, being responsive and interesting. Interpretation and judgmental biases in social phobia - Voncken Article (2003) Introduction Psychopathology Page 10 Interpretation bias - the interpretation of ambiguous events as negative. It may be specifically involved in those anxiety disorders in which ambiguous information needs to be disambiguated (e.g. SAD). Interpretation bias in SAD is content-specific, i.e. SAD patients show a negative interpretations only for social, but not for non-social events (compared to normal subjects and patients with other anxiety disorders). Non-ambiguous slightly negative events (e.g. 'he is not really interested in what you're saying') are catastrophized by SAD patients => these are also subject to interpretation bias. Judgmental bias - the overestimation of the costs and/or probability of a negative event. SAD patients have a judgmental bias, which is also content-specific. It has been argued that SAD patients are afraid of highly probable events (e.g. stuttering), while patients with other anxiety disorders are afraid of less probable events, e.g. heart attack (panic disorder) or having an accident (OCD). Therefore, it is suggested that SAD is distinguished by exaggerated cost estimations, while other anxiety disorders are more distinguished by exaggerated probability estimations. ○ Results for this are conflicting. The present study investigates interpretation bias and judgmental bias in SAD patients and healthy controls. Method Participants are presented with social events. To assess interpretation bias, participants arrange 4 different interpretations on likelihood. These interpretations range from positive, neutral, mildly negative to profoundly negative. To assess judgmental bias, the estimations of probability and costs of the profoundly negative interpretation (e.g. 'negative evaluation by others') are recorded. These estimations were converted into a threat score. Hypothesis: SAD patients will show content-specific interpretation and judgmental biases. In other words, compared to normal controls they will: Interpret social events as more negative and will give higher cost & probability ratings of a profoundly negative interpretation in social events, and thus judge social events as more threatening. They will not differ in their ratings of non-social events. Show interpretation & judgmental biases in social events of different valence (positive, ambiguous, mildly negative & profoundly negative). Differ from normal controls more for cost than for probability ratings of a negative evaluation in social events. Interpretation and Judgmental Questionnaire (IJQ) - consists of 20 scripts of social events and 4 non-social control events, ranging from positive (e.g. Someone makes a compliment about your looks), ambiguous (Somebody you know looks in your direction), mildly negative (The newly introduced person doesn't say anything to you) to profoundly negative (A friend tells you that a colleague dislikes you). This questionnaire was used to assess interpretation & judgmental bias. Results & discussion For social events, SAD patients had higher ratings than controls, while for non-social events no difference was found between groups. Interpretation and judgmental biases were present in social events of different valence (positive, ambiguous, mildly & profou ndly negative). SAD patients did not have the tendency to overestimate costs over probability of negative social evaluation compared to controls. Hypotheses 1 and 2 were confirmed by the results. Hypothesis 3 was not confirmed => the results do not support the idea that SAD patients overestimate costs and not so much pr obability of mildly negative social events. Appendix: DSM-5 criteria for SAD (left) & Panic disorder (right) Psychopathology Page 11 Psychopathology Page 12