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Impulsivity and aggression mediate regional brain responses in Borderline Personality Disorder: An fMRI study

机译:冲动和侵略介导区域脑反应在边界人格障碍中:一个FMRI研究

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Fronto-limbic brain networks involved in regulation of impulsivity and aggression are abnormal in Borderline Personality Disorder (BPD). However, it is unclear whether, or to what extent, these personality traits actually modulate brain responses during cognitive processing. Using fMRI, we examined the effects of trait impulsivity, aggression, and depressed mood on regional brain responses in 31 female BPD and 25 control subjects during a Go No-Go task using Ekman faces as targets. First-level contrasts modeled effects of negative emotional context. Second-level regression models used trait impulsivity, aggression and depressed mood as predictor variables of regional brain activations. In BPD, trait impulsivity was positively correlated with activation in the dorsal anterior cingulate cortex, orbital frontal cortex (OFC), basal ganglia (BG), and dorsolateral prefrontal cortex, with no areas of negative correlation. In contrast, aggression was negatively correlated with activation in OFC, hippocampus, and BG, with no areas of positive correlation. Depressed mood had a generally dampening effect on activations. Effects of trait impulsivity on healthy controls differed from effects in BPD, suggesting a disorder-specific response. Negative emotional context and trait impulsivity, but not aggression or depression, diminished task performance across both groups. Negative emotional context may interfere with cognitive functioning in BPD through interaction with the neurobiology of personality traits.
机译:涉及冲动和侵蚀的调节的前肢脑网络在边界人格障碍(BPD)中异常。然而,目前尚不清楚这些人格特征是否在认知处理期间实际调节脑响应。使用FMRI,我们检查了在GO NO-GO TRUAT期间使用EKMAN面对目标的GO NO-GO-TAGE中的31名女性BPD和25个对照科目的区域脑响应的影响。第一级对比对否定情绪背景的建模效应。二级回归模型使用特质冲击,侵略和抑郁情绪作为区域脑激活的预测变量。在BPD中,性状冲击与背侧铰接皮质,眶正面皮质(OFC),基底神经节(BG)和背面层前额叶皮质的激活呈正相关,没有负相关区域。相比之下,侵略性与OFC,海马和BG的激活是伴随的,没有正相关区域。抑郁的情绪对激活产生了一般抑制效果。特质冲动对健康对照的影响与BPD的效果不同,表明特异性疾病的反应。负面情绪背景和特性冲动,但不是侵略或抑郁,两组任务表现减少。阴性情绪背景可能通过与人格特征的神经生物学的相互作用来干扰BPD中的认知功能。

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