Department of Clinical Psychology, Universidad de Granada, Spain.
Eur Neuropsychopharmacol. 2013 Dec;23(12):1698-707. doi: 10.1016/j.euroneuro.2013.04.012. Epub 2013 May 25.
Cocaine dependence often co-occurs with Cluster B personality disorders. Since both disorders are characterized by emotion regulation deficits, we predicted that cocaine comorbid patients would exhibit dysfunctional patterns of brain activation and connectivity during reappraisal of negative emotions. We recruited 18 cocaine users with comorbid Cluster B personality disorders, 17 cocaine users without comorbidities and 21 controls to be scanned using functional magnetic resonance imaging (fMRI) during performance on a reappraisal task in which they had to maintain or suppress the emotions induced by negative affective stimuli. We followed region of interest (ROI) and whole-brain approaches to investigate brain activations and connectivity associated with negative emotion experience and reappraisal. Results showed that cocaine users with comorbid personality disorders had reduced activation of the subgenual anterior cingulate cortex during negative emotion maintenance and increased activation of the lateral orbitofrontal cortex and the amygdala during reappraisal. Amygdala activation correlated with impulsivity and antisocial beliefs in the comorbid group. Connectivity analyses showed that in the cocaine comorbid group the subgenual cingulate was less efficiently connected with the amygdala and the fusiform gyri and more efficiently connected with the anterior insula during maintenance, whereas during reappraisal the left orbitofrontal cortex was more efficiently connected with the amygdala and the right orbitofrontal cortex was less efficiently connected with the dorsal striatum. We conclude that cocaine users with comorbid Cluster B personality disorders have distinctive patterns of brain activation and connectivity during maintenance and reappraisal of negative emotions, which correlate with impulsivity and dysfunctional beliefs.
可卡因依赖常与 B 群人格障碍共病。由于这两种疾病的特征都是情绪调节缺陷，我们预测可卡因共病患者在重新评估负面情绪时会表现出大脑激活和连接的功能失调模式。我们招募了 18 名可卡因使用者，他们有共病 B 群人格障碍，17 名可卡因使用者没有共病，21 名对照者，让他们在进行重新评估任务时接受功能磁共振成像（fMRI）扫描，在这个任务中，他们必须保持或抑制负面情感刺激引起的情绪。我们采用了基于感兴趣区域（ROI）和全脑的方法来研究与负面情绪体验和重新评估相关的大脑激活和连接。结果表明，可卡因使用者有共病人格障碍时，在负面情绪维持期间，前扣带回皮质的亚属区活动减少，在重新评估期间，外侧眶额皮质和杏仁核的活动增加。杏仁核的活动与共病组的冲动和反社会信念相关。连接分析显示，在可卡因共病组中，亚属扣带在维持期间与杏仁核和梭状回的连接效率较低，与前岛叶的连接效率较高，而在重新评估期间，左侧眶额皮质与杏仁核的连接效率较高，右侧眶额皮质与背侧纹状体的连接效率较低。我们得出结论，可卡因使用者有共病 B 群人格障碍时，在维持和重新评估负面情绪时，大脑的激活和连接模式有独特之处，这与冲动和功能失调的信念相关。
