scholarly journals Korean Guidelines for the Pharmacological Treatment of Social Anxiety Disorder: Initial Treatment Strategies

2018 ◽  
Vol 15 (2) ◽  
pp. 147-155
Author(s):  
Hyungkun Yoon ◽  
Dong Jae Oh ◽  
Ho-Suk Suh ◽  
Kyoung-Uk Lee ◽  
Se-Won Lim ◽  
...  
Keyword(s):  
Anxiety Disorder ◽  
Social Anxiety ◽  
Social Anxiety Disorder ◽  
Pharmacological Treatment ◽  
Initial Treatment ◽  
Treatment Strategies

scholarly journals A pilot study of clonazepam versus psychodynamic group therapy plus clonazepam in the treatment of generalized social anxiety disorder

2008 ◽  
Vol 23 (8) ◽  
pp. 567-574 ◽  
Author(s):  
Daniela Z. Knijnik ◽  
Carlos Blanco ◽  
Giovanni Abrahão Salum ◽  
Carolina U. Moraes ◽  
Clarissa Mombach ◽  
...  
Keyword(s):  
Anxiety Disorder ◽  
Social Anxiety ◽  
Group Therapy ◽  
Social Anxiety Disorder ◽  
Treatment Strategies ◽  
World Health ◽  
Global Functioning ◽  
Psychodynamic Group Therapy ◽  
Efficacy Measures ◽  
Health Organization

AbstractBackgroundBoth psychodynamic group therapy (PGT) and clonazepam are used as treatment strategies in reducing symptoms of generalized social anxiety disorder (GSAD). However, many individuals remain symptomatic after treatment with PGT or clonazepam.MethodFifty-eight adult outpatients with a diagnosis of GSAD according to DSM-IV were randomized to 12 weeks PGT plus clonazepam or clonazepam. The Clinical Global Impression-Improvement (CGI-I) Scale was the primary efficacy measure. Secondary efficacy measures included the Liebowitz Social Anxiety Scale (LSAS) total score, the World Health Organization Instrument to Assess Quality of Life—Brief (WHOQOL-Bref) Scale and the Beck Depression Inventory (BDI).ResultsCGI-I data from 57 patients (intent-to-treat population) showed that patients who received PGT plus clonazepam presented significantly greater improvement than those who received clonazepam (P = 0.033). There were no significant differences between the two groups in the secondary efficacy measures.ConclusionsOur study suggests that the combination of PGT with clonazepam may be a promising strategy for the treatment of GSAD, regarding gains in the global functioning. However the present study failed to detect more specific changes in social anxiety symptomatology between the two groups.

Pediatric Social Anxiety Disorder: Predictors of Response to Pharmacological Treatment

2012 ◽  
Vol 22 (6) ◽  
pp. 410-414 ◽  
Author(s):  
Gabriele Masi ◽  
Chiara Pfanner ◽  
Maria Mucci ◽  
Stefano Berloffa ◽  
Angela Magazù ◽  
...  
Keyword(s):  
Anxiety Disorder ◽  
Social Anxiety ◽  
Social Anxiety Disorder ◽  
Pharmacological Treatment ◽  
Predictors Of Response

Integrating Neurobiology and Psychopathology into Evidence-Based Treatment of Social Anxiety Disorder

CNS Spectrums ◽  
2005 ◽  
Vol 10 (S13) ◽  
pp. 1-2 ◽  
Author(s):  
Michael R. Liebowitz ◽  
Philip T. Ninan ◽  
Franklin R. Schneier ◽  
Carlos Blanco ◽  
David L. Ginsberg ◽  
...  
Keyword(s):  
Anxiety Disorder ◽  
Social Anxiety ◽  
Social Anxiety Disorder ◽  
Selective Serotonin Reuptake Inhibitors ◽  
Treatment Strategies ◽  
Psychosocial Treatment ◽  
Development Theory ◽  
Future Research ◽  
Life Issues ◽  
Neuroreceptor Imaging

AbstractSocial anxiety disorder (SAD) is a common, chronic psychiatric disorder characterized by a persistent fear of social or performance situations in which embarrassment can occur. This disorder typically appears during the mid-adolescent years and is unremitting throughout life if not properly treated. SAD presents as two subtypes: the more common and debilitating generalized form, and the nongeneralized form, which consists predominantly of performance anxiety. The majority of patients with SAD have comorbid mental disorders, including mood, anxiety, and substance abuse. No single development theory has been proposed to account for the origins of SAD, although current understanding of the etiology of SAD posits an interaction between psychological and biological factors. Risk factors include environmental and parenting influences and dysfunctional cognitive and conditioning events in early childhood. The neurobiology of SAD appears to involve neurochemical dysfunction, as evidenced by studies of neuroreceptor imaging, neuroendocrine function, and profiles of response to specific medications. Clinical trials have demonstrated that benzodiazepines and antidepressants are effective in the treatment of SAD. The selective serotonin reuptake inhibitors are emerging as the first-line treatment for SAD, based on their proven safety, tolerability, and efficacy. Goals for ongoing future research include development of approaches to achieve remission, to convert nonresponders and partial responders to full responders, and to prevent relapse and maintain long-term efficacy.This monograph explores the epidemiology, clinical presentation, and differential diagnosis of SAD, with a focus on neural circuitry of social relationships and neurochemical dysfunction. The prevalence, rates of recognition and treatment, patterns of comorbidity, quality-of-life issues, and natural history of SAD are discussed as well as pharmacologic and psychosocial treatment strategies for SAD.

scholarly journals The evidence-based pharmacological treatment of social anxiety disorder

2003 ◽  
Vol 6 (4) ◽  
pp. 427-442 ◽  
Author(s):  
Carlos Blanco ◽  
Muhammad S. Raza ◽  
Franklin R. Schneier ◽  
Michael R. Liebowitz
Keyword(s):  
Anxiety Disorder ◽  
Social Anxiety ◽  
Social Anxiety Disorder ◽  
Pharmacological Treatment ◽  
Evidence Based

Integrating Neurobiology and Psychopathology into Evidence-Based Treatment of Social Anxiety Disorder

CNS Spectrums ◽  
2005 ◽  
Vol 10 (10) ◽  
pp. 805a-805b ◽  
Author(s):  
Michael R. Liebowitz ◽  
David L. Ginsberg ◽  
Philip T. Ninan ◽  
Franklin R. Schneier ◽  
Carlos Blanco
Keyword(s):  
Anxiety Disorder ◽  
Social Anxiety ◽  
Social Anxiety Disorder ◽  
Selective Serotonin Reuptake Inhibitors ◽  
Treatment Strategies ◽  
Psychosocial Treatment ◽  
Development Theory ◽  
Future Research ◽  
Life Issues ◽  
Neuroreceptor Imaging

AbstractSocial anxiety disorder (SAD) is a common, chronic psychiatric disorder characterized by a persistent fear of social or performance situations in which embarrassment can occur. This disorder typically appears during the mid-adolescent years and is unremitting throughout life if not properly treated. SAD presents as two subtypes: the more common and debilitating generalized form, and the nongeneralized form, which consists predominantly of performance anxiety. The majority of patients with SAD have comorbid mental disorders, including mood, anxiety, and substance abuse. No single development theory has been proposed to account for the origins of SAD, although current understanding of the etiology of SAD posits an interaction between psychological and biological factors. Risk factors include environmental and parenting influences and dysfunctional cognitive and conditioning events in early childhood. The neurobiology of SAD appears to involve neurochemical dysfunction, as evidenced by studies of neuroreceptor imaging, neuroendocrine function, and profiles of response to specific medications. Clinical trials have demonstrated that benzodiazepines and antidepressants are effective in the treatment of SAD. The selective serotonin reuptake inhibitors are emerging as the first-line treatment for SAD, based on their proven safety, tolerability, and efficacy. Goals for ongoing future research include development of approaches to achieve remission, to convert nonresponders and partial responders to full responders, and to prevent relapse and maintain long-term efficacy.This monograph explores the epidemiology, clinical presentation, and differential diagnosis of SAD, with a focus on neural circuitry of social relationships and neurochemical dysfunction. The prevalence, rates of recognition and treatment, patterns of comorbidity, quality-of-life issues, and natural history of SAD are discussed as well as pharmacologic and psychosocial treatment strategies for SAD.

scholarly journals The evidence-based pharmacotherapy of social anxiety disorder

2013 ◽  
Vol 16 (1) ◽  
pp. 235-249 ◽  
Author(s):  
Carlos Blanco ◽  
Laura B. Bragdon ◽  
Franklin R. Schneier ◽  
Michael R. Liebowitz
Keyword(s):  
Anxiety Disorder ◽  
Social Anxiety ◽  
Monoamine Oxidase ◽  
Social Anxiety Disorder ◽  
Pharmacological Treatment ◽  
Selective Serotonin Reuptake Inhibitors ◽  
Monoamine Oxidase A ◽  
Treatment Resistant ◽  
First Line ◽  
First Line Therapy

Abstract Social anxiety disorder (SAD) is a highly prevalent and often disabling disorder. This paper reviews the pharmacological treatment of SAD based on published placebo-controlled studies and published meta-analyses. It addresses three specific questions: What is the first-line pharmacological treatment of SAD? How long should treatment last? What should be the management of treatment-resistant cases? Based on their efficacy for SAD and common co-morbid disorders, tolerability and safety, selective serotonin reuptake inhibitors (SSRIs) and venlafaxine should be considered the first-line treatment for most patients. Less information is available regarding the optimal length of treatment, although individuals who discontinue treatment after 12–20 wk appear more likely to relapse than those who continue on medication. Even less empirical evidence is available to support strategies for treatment-resistant cases. Clinical experience suggests that SSRI non-responders may benefit from augmentation with benzodiazepines or gabapentin or from switching to monoamine oxidase inhibitors, reversible inhibitors of monoamine oxidase A, benzodiazepines or gabapentin. Cognitive-behavioural is a well-established alternative first line therapy that may also be a helpful adjunct in non-responders to pharmacological treatment of SAD.

Pharmacological Treatment for Social Anxiety Disorder

2014 ◽  
pp. 521-546 ◽  
Author(s):  
Franklin R. Schneier ◽  
Laura B. Bragdon ◽  
Carlos Blanco ◽  
Michael R. Liebowitz
Keyword(s):  
Anxiety Disorder ◽  
Social Anxiety ◽  
Social Anxiety Disorder ◽  
Pharmacological Treatment
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