____________________________________________________________________________ Anxiety Disorders
in panic disorder with agoraphobia and serotonergic system relevance in mediating the connection between balance and agoraphobia [298]. The authors suggest that real abnormal body functioning (primarily involving cardiorespiratory and balance systems), which leads to reduced overall physical fit- ness, may be a primary cause of panic disorder and that the anxiety and fear it induces is sustained by repeated signals of impaired body functioning [299]. In one study, patients with panic disorder/agoraphobia received alprazolam plus exposure, alprazolam plus progres- sive muscle relaxation, placebo plus exposure, or placebo plus progressive muscle relaxation. The highest rate of improvement at follow-up was observed in the placebo/exposure (71%) and alprazolam/exposure (71%) groups; alprazolam/progressive muscle relaxation (51%) and progressive muscle relaxation/ placebo (25%) groups were less improved [300]. Alprazolam showed no benefit over placebo when added to exposure therapy as treatment for panic disorder/agoraphobia [300]. CONTRIBUTING FACTORS TO PANIC DISORDER WITH AGORAPHOBIA TREATMENT RESPONSE Pronounced safety behaviors during exposure therapy, but not at baseline, have been associated with poor treatment response in patients with panic disorder/agoraphobia. This underscores the importance of rigorous safety behavior assessment during therapy [301]. During 13 to 21 years post-treatment follow-up, major depres- sion at baseline predicted worse improvement in agoraphobic avoidance in the first year. Employment and marriage/cohabi- tation at baseline predicted greater improvement at 1-year, 2-year, and 13- to 21-year follow-up [302]. A substantial number of patients with panic disorder/agora- phobia fail to improve following CBT. Agoraphobic avoidance is the most consistent predictor of decreased improvement, followed by low expectancy for change, high levels of functional impairment, and Cluster C personality pathology [303].
with pharmacotherapy. CBT for SAD can be administered in group or individual formats. Although some studies have reported that individual CBT is superior to group CBT, meta- analyses have failed to find significant differences in efficacy between the two modalities. There is evidence to support the effectiveness of exposure therapy alone, but efficacy compared with CBT is equivocal [120]. Several CBT variants have been examined. Videotaped feed- back was not shown to enhance the effects of exposure-based treatment. However, CBT with virtual reality exposure was found more effective than wait-list control and as effective as CBT with imaginal or in vivo exposure according to two meta-analyses [120]. A form of CBT focused on interpersonal behavior found simi- lar improvements in social anxiety compared to standard CBT and also increased relationship satisfaction and social approach behaviors. Evidence to support interpersonal therapy in SAD is conflicting; while some results are negative, interpersonal therapy is probably more effective than wait-list control, but less effective than traditional CBT [120]. With Internet CBT for SAD, patients with an avoidance and depression profile showed lower remission after treatment, higher levels of social anxiety at follow-up assessments, and typi- cally remained highly symptomatic. In patients with SAD, high levels of social avoidance and depressive symptoms constitute a risk profile for poor treatment response [304]. PHARMACOTHERAPY Pharmacotherapy of SAD is effective but varies considerably, with room for further improvement [305]. Placebo-controlled clinical trials have shown that SSRIs and SNRIs are the most effective class of pharmacologic treatment. The ADAC recom- mends escitalopram, fluvoxamine (immediate- or controlled- release), paroxetine (immediate- or controlled-release), pre- gabalin, sertraline, or venlafaxine XR for first-line treatment of SAD [120]. Citalopram has less evidence but is likely as effective as other SSRIs. Phenelzine efficacy is established in multiple randomized controlled trials but is recommended as a second-line option due to concerns over dietary and medi- cation restrictions that, if not strictly adhered to, can lead to hypertensive crisis [120]. Abnormalities in brain GABA and glutamate systems have been studied in patients with SAD, including whether these changed following eight weeks of levetiracetam. Compared to healthy controls, patients with SAD at baseline showed signifi- cantly higher whole brain levels of glutamate and glutamine (but not GABA) and significantly higher thalamic glutamine and lower GABA levels. Following treatment, these patients showed significant reduction in thalamic glutamine. These findings support the role of impaired GABAergic and over- active glutamatergic function in SAD and may explain the anxiolytic effects of levetiracetam [306].
TREATMENT OF SOCIAL ANXIETY DISORDER
PSYCHOTHERAPY CBT is the criterion-standard psychologic treatment for SAD. Cognitive restructuring techniques are used to challenge assumptions and maladaptive thoughts (i.e., “I will embarrass myself”), while the behavioral component centers on patient exposure to anxiety-provoking situations. Over time and with repeated exposure sessions, the goal is to reduce anxiety symp- toms and to demonstrate that the situational anxiety is toler- able and without substantial risk. The efficacy of CBT is sup- ported by many randomized controlled trials, with outcomes that vary but are typically similar to pharmacotherapy. Some reports suggest that, after treatment discontinuation, gains achieved with CBT may persist longer than those achieved
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