Cohen Jonah N, Potter Carrie M, Drabick Deborah A G, Blanco Carlos, Schneier Franklin R, Liebowitz Michael R, Heimberg Richard G
Department of Psychology, Weiss Hall, Temple University, 1701 North 13th Street, Philadelphia, PA 19122, USA.
Department of Psychiatry, Columbia University, Harness Pavilion, 180 Ft. Washington Avenue, New York, NY 10032, USA; New York State Psychiatric Institute, 1051 Riverside Drive, New York, NY 10032, USA.
Psychiatry Res. 2015 Jul 30;228(1):65-71. doi: 10.1016/j.psychres.2015.04.014. Epub 2015 Apr 16.
Therapies for social anxiety disorder (SAD) leave many patients symptomatic at the end of treatment and little is known about predictors of treatment response. This study investigated the predictive relationship of patients' etiological attributions to initial clinical features and response to pharmacotherapy. One hundred thirty-seven individuals seeking treatment for SAD received 12 weeks of open treatment with paroxetine. Participants completed the Attributions for the Etiology of Social Anxiety Scale at baseline in addition to measures of social anxiety and depression at baseline and over the course of treatment. A latent class analysis suggested four profiles of etiological beliefs about one's SAD that may be characterized as: Familial Factors, Need to be Liked, Bad Social Experiences, and Diffuse Beliefs. Patients in the more psychosocially-driven classes, Need to be Liked and Bad Social Experiences, had the most severe social anxiety and depression at baseline. Patients in the Familial Factors class, who attributed their SAD to genetic, biological, and early life experiences, had the most rapid response to paroxetine.These results highlight the effect of biological and genetically-oriented etiological beliefs on pharmacological intervention, have implications for person-specific treatment selection, and identify potential points of intervention to augment treatment response.
社交焦虑障碍（SAD）的治疗方法在治疗结束时仍使许多患者有症状，而且对于治疗反应的预测因素知之甚少。本研究调查了患者的病因归因与初始临床特征及药物治疗反应之间的预测关系。137名寻求SAD治疗的个体接受了为期12周的帕罗西汀开放治疗。参与者在基线时完成了社交焦虑病因量表的归因，此外还在基线和治疗过程中完成了社交焦虑和抑郁的测量。潜在类别分析表明，关于自身SAD的病因信念有四种类型，可能被描述为：家族因素、需要被喜欢、不良社交经历和弥散信念。在心理社会驱动较强的类别（需要被喜欢和不良社交经历）中的患者在基线时社交焦虑和抑郁最为严重。将其SAD归因于遗传、生物学和早期生活经历的家族因素类别中的患者对帕罗西汀反应最快。这些结果突出了生物学和基因导向的病因信念对药物干预的影响，对个性化治疗选择有启示意义，并确定了增强治疗反应的潜在干预点。
