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创伤后应激障碍的脑成像

Brain imaging in posttraumatic stress disorder.

作者信息

Villarreal G, King C Y

机构信息

Department of Psychiatry, University of New Mexico, Albuquerque, NM 87131, USA.

出版信息

Semin Clin Neuropsychiatry. 2001 Apr;6(2):131-45. doi: 10.1053/scnp.2001.21840.

DOI:10.1053/scnp.2001.21840
PMID:11296313
Abstract

This is a review article of neuroimaging studies in post-traumatic stress disorder (PTSD). Findings from structural, biochemical, and functional studies are summarized. Magnetic resonance imaging (MRI) volumetric studies have consistently reported decreased hippocampal volumes in PTSD. Proton magnetic resonance spectroscopy studies report decreased N-acetyl aspartate (NAA) ratios and absolute concentrations in the medial temporal lobe. Although still controversial, these findings from volumetric and spectroscopic studies are thought to represent decreased neuronal density of the hippocampus. Functional imaging studies document different patterns of limbic and paralimbic structure activation in PTSD compared with controls. Of theoretical importance are findings of failure to activate the anterior cingulate as well as amygdala activation during symptom provocation studies. Also, increased amygdala activation was found with a behavioral task targeted to this structure. A neurobiological model is presented that takes into account findings from neuroimaging studies in PTSD as well as animal studies of fear conditioning. This model proposes that central to symptom mediation is a dysfunction of the anterior cingulate, with a failure to inhibit amygdala activation and/or an intrinsic lower threshold of amygdala response to fearful stimuli. The model further proposes that hippocampal atrophy is a result of the chronic hyperarousal symptoms mediated by amygdala activation.

摘要

这是一篇关于创伤后应激障碍(PTSD)神经影像学研究的综述文章。总结了结构、生化和功能研究的结果。磁共振成像(MRI)体积研究一直报告PTSD患者海马体积减小。质子磁共振波谱研究报告内侧颞叶中N-乙酰天门冬氨酸(NAA)比率和绝对浓度降低。尽管仍存在争议,但这些体积和波谱研究的结果被认为代表海马神经元密度降低。功能成像研究表明,与对照组相比,PTSD患者边缘和边缘旁结构激活模式不同。在症状激发研究中未能激活前扣带回以及杏仁核激活的发现具有理论重要性。此外,针对该结构的行为任务发现杏仁核激活增加。本文提出了一个神经生物学模型,该模型考虑了PTSD神经影像学研究以及恐惧条件反射动物研究的结果。该模型提出,症状调节的核心是前扣带回功能障碍,无法抑制杏仁核激活和/或杏仁核对恐惧刺激的内在较低反应阈值。该模型进一步提出,海马萎缩是杏仁核激活介导的慢性过度觉醒症状的结果。

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