Posttraumatic stress disorder: the role of medial prefrontal cortex and amygdala.
Posttraumatic stress disorder: the role of medial prefrontal cortex and amygdala.
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DOI：
10.1177/1073858409333072
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发表时间：
2009-10
期刊：
影响因子：
--
通讯作者：
Grafman J
中科院分区：
文献类型：
--
作者：
Koenigs M;Grafman J
创伤后应激障碍（PTSD）的特征是反复出现对情感创伤事件的痛苦记忆。在这篇综述中，我们展示了两个大脑区域——杏仁核和腹内侧前额叶皮层（vmPFC）——在创伤后应激障碍和相关情绪过程中的功能。一系列人类和非人类研究表明，杏仁核介导条件性恐惧的获得和表达以及情绪记忆的增强，而vmPFC介导条件性恐惧的消除和消极情绪的意志调节。从理论上讲，vmPFC对杏仁核有抑制作用，这种抑制作用的缺陷可以解释PTSD的症状。这一理论得到了创伤后应激障碍患者的功能成像研究的支持，这些患者表现出vmPFC低活性而杏仁核高活性。最近一项针对脑损伤和创伤暴露的退伍军人的研究证实，杏仁核损伤降低了患创伤后应激障碍的可能性。但与自上而下抑制模型的预测相反，vmPFC损伤也降低了患PTSD的可能性。根据这些结果，讨论了杏仁核和vmPFC在创伤后应激障碍病理生理中的作用，以及对潜在治疗的影响。
Post-traumatic stress disorder (PTSD) is characterized by recurrent distressing memories of an emotionally traumatic event. In this review, we present neuroscientific data highlighting the function of two brain areas—the amygdala and ventromedial prefrontal cortex (vmPFC)—in PTSD and related emotional processes. A convergent body of human and non-human studies suggests that the amygdala mediates the acquisition and expression of conditioned fear and the enhancement of emotional memory, whereas the vmPFC mediates the extinction of conditioned fear and the volitional regulation of negative emotion. It has been theorized that the vmPFC exerts inhibition on the amygdala, and that a defect in this inhibition could account for the symptoms of PTSD. This theory is supported by functional imaging studies of PTSD patients, who exhibit hypoactivity in vmPFC but hyperactivity in amygdala. A recent study of brain-injured and trauma-exposed combat veterans confirms that amygdala damage reduces the likelihood of developing PTSD. But contrary to the prediction of the top-down inhibition model, vmPFC damage also reduces the likelihood of developing PTSD. The putative roles of amygdala and vmPFC in the pathophysiology of PTSD, as well as implications for potential treatments, are discussed in light of these results.
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