Cremers Henk R, Veer Ilya M, Spinhoven Philip, Rombouts Serge A R B, Roelofs Karin
Radboud University Nijmegen, Behavioral Science Institute Nijmegen, Netherlands ; Biological Science Department, Department of Psychiatry, University of Chicago Chicago, IL, USA ; Leiden Institute for Brain and Cognition Leiden, Netherlands.
Leiden Institute for Brain and Cognition Leiden, Netherlands ; Department of Radiology, Leiden University Medical Center Leiden, Netherlands ; Division of Mind and Brain Research, Department of Psychiatry and Psychotherapy, Charité Universitätsmedizin Berlin, Germany.
Front Behav Neurosci. 2015 Jan 5;8:439. doi: 10.3389/fnbeh.2014.00439. eCollection 2014.
An imbalance in the neural motivational system may underlie Social Anxiety Disorder (SAD). This study examines social reward and punishment anticipation in SAD, predicting a valence-specific effect: increased striatal activity for punishment avoidance compared to obtaining a reward. Individuals with SAD (n = 20) and age, gender, and education case-matched controls (n = 20) participated in a functional magnetic resonance imaging (fMRI) study. During fMRI scanning, participants performed a Social Incentive Delay (SID) task to measure the anticipation of social reward and punishment. The left putamen (part of the striatum) showed a valence-specific interaction with group after correcting for medication use and comorbidity. The control group showed a relatively stronger activation for reward vs. punishment trials, compared to the social anxiety group. However, post-hoc pairwise comparisons were not significant, indicating that the effect is driven by a relative difference. A connectivity analysis (Psychophysiological interaction) further revealed a general salience effect: SAD patients showed decreased putamen-ACC connectivity compared to controls for both reward and punishment trials. Together these results suggest that the usual motivational preference for social reward is absent in SAD. In addition, cortical control processes during social incentive anticipation may be disrupted in SAD. These results provide initial evidence for altered striatal involvement in both valence-specific and valence-nonspecific processing of social incentives, and stress the relevance of taking motivational processes into account when studying social anxiety.
神经动机系统的失衡可能是社交焦虑障碍（SAD）的潜在原因。本研究考察了社交焦虑障碍患者对社交奖励和惩罚的预期，预测了一种效价特异性效应：与获得奖励相比，为避免惩罚纹状体活动增加。20名社交焦虑障碍患者和20名年龄、性别及教育程度相匹配的对照者参与了一项功能磁共振成像（fMRI）研究。在fMRI扫描期间，参与者执行一项社会激励延迟（SID）任务，以测量对社交奖励和惩罚的预期。在校正药物使用和共病因素后，左侧壳核（纹状体的一部分）显示出与组别之间的效价特异性交互作用。与社交焦虑组相比，对照组在奖励试验与惩罚试验中表现出相对更强的激活。然而，事后两两比较并不显著，表明该效应是由相对差异驱动的。一项连接性分析（心理生理交互作用）进一步揭示了一种普遍的显著性效应：在奖励和惩罚试验中，与对照组相比，社交焦虑障碍患者壳核与前扣带回的连接性均降低。这些结果共同表明，社交焦虑障碍患者缺乏对社交奖励通常的动机偏好。此外，社交激励预期期间的皮层控制过程在社交焦虑障碍中可能受到干扰。这些结果为纹状体在社交激励的效价特异性和非特异性加工中参与的改变提供了初步证据，并强调了在研究社交焦虑时考虑动机过程的相关性。
