Britton Jennifer C, Suway Jenna G, Clementi Michelle A, Fox Nathan A, Pine Daniel S, Bar-Haim Yair
Section on Development and Affective Neuroscience, National Institute of Mental Health, Bethesda, MD, 20892 USA, Department of Psychology, University of Miami, Coral Gables, FL, 33146 USA, Department of Human Development and Quantitative Methodology, University of Maryland, College Park, MD, 20742 USA, Joint Doctoral Program in Clinical Psychology, San Diego State University/University of California, San Diego, San Diego, CA, 92120 USA, Department of Psychology, University of Houston, Houston, TX, 77204 USA, and School of Psychological Sciences and Sagol School of Neuroscience, Tel Aviv University, Tel Aviv, 69978 Israel Section on Development and Affective Neuroscience, National Institute of Mental Health, Bethesda, MD, 20892 USA, Department of Psychology, University of Miami, Coral Gables, FL, 33146 USA, Department of Human Development and Quantitative Methodology, University of Maryland, College Park, MD, 20742 USA, Joint Doctoral Program in Clinical Psychology, San Diego State University/University of California, San Diego, San Diego, CA, 92120 USA, Department of Psychology, University of Houston, Houston, TX, 77204 USA, and School of Psychological Sciences and Sagol School of Neuroscience, Tel Aviv University, Tel Aviv, 69978 Israel
Section on Development and Affective Neuroscience, National Institute of Mental Health, Bethesda, MD, 20892 USA, Department of Psychology, University of Miami, Coral Gables, FL, 33146 USA, Department of Human Development and Quantitative Methodology, University of Maryland, College Park, MD, 20742 USA, Joint Doctoral Program in Clinical Psychology, San Diego State University/University of California, San Diego, San Diego, CA, 92120 USA, Department of Psychology, University of Houston, Houston, TX, 77204 USA, and School of Psychological Sciences and Sagol School of Neuroscience, Tel Aviv University, Tel Aviv, 69978 Israel Section on Development and Affective Neuroscience, National Institute of Mental Health, Bethesda, MD, 20892 USA, Department of Psychology, University of Miami, Coral Gables, FL, 33146 USA, Department of Human Development and Quantitative Methodology, University of Maryland, College Park, MD, 20742 USA, Joint Doctoral Program in Clinical Psychology, San Diego State University/University of California, San Diego, San Diego, CA, 92120 USA, Department of Psychology, University of Houston, Houston, TX, 77204 USA, and School of Psychological Sciences and Sagol School of Neuroscience, Tel Aviv University, Tel Aviv, 69978 Israel.
Soc Cogn Affect Neurosci. 2015 Jul;10(7):913-20. doi: 10.1093/scan/nsu141. Epub 2014 Oct 24.
Attention bias modification (ABM) procedures typically reduce anxiety symptoms, yet little is known about the neural changes associated with this behavioral treatment. Healthy adults with high social anxiety symptoms (n = 53) were randomized to receive either active or placebo ABM. Unlike placebo ABM, active ABM aimed to train individuals' attention away from threat. Using the dot-probe task, threat-related attention bias was measured during magnetic resonance imaging before and after acute and extended training over 4 weeks. A subset of participants completed all procedures (n = 30, 15 per group). Group differences in neural activation were identified using standard analyses. Linear regression tested predictive factors of symptom reduction (i.e., training group, baseline indices of threat bias). The active and placebo groups exhibited different patterns of right and left amygdala activation with training. Across all participants irrespective of group, individuals with greater left amygdala activation in the threat-bias contrast prior to training exhibited greater symptom reduction. After accounting for baseline amygdala activation, greater symptom reduction was associated with assignment to the active training group. Greater left amygdala activation at baseline predicted reductions in social anxiety symptoms following ABM. Further research is needed to clarify brain-behavior mechanisms associated with ABM training.
注意偏向矫正（ABM）程序通常会减轻焦虑症状，但对于这种行为治疗相关的神经变化却知之甚少。具有高社交焦虑症状的健康成年人（n = 53）被随机分为接受主动或安慰剂ABM组。与安慰剂ABM不同，主动ABM旨在训练个体将注意力从威胁上转移开。使用点探测任务，在4周的急性和延长训练前后的磁共振成像期间测量与威胁相关的注意偏向。一部分参与者完成了所有程序（n = 30，每组15人）。使用标准分析确定神经激活的组间差异。线性回归测试了症状减轻的预测因素（即训练组、威胁偏向的基线指标）。随着训练，主动组和安慰剂组在左右杏仁核激活方面表现出不同的模式。在所有参与者中，无论组别如何，在训练前威胁偏向对比中左侧杏仁核激活程度较高的个体症状减轻程度更大。在考虑了基线杏仁核激活后，更大程度的症状减轻与被分配到主动训练组有关。基线时左侧杏仁核激活程度较高可预测ABM训练后社交焦虑症状的减轻。需要进一步的研究来阐明与ABM训练相关的脑-行为机制。
