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重度抑郁症中的前额叶皮质-杏仁核代谢

Prefrontal cortical-amygdalar metabolism in major depression.

作者信息

Drevets W C

机构信息

Department of Psychiatry, University of Pittsburgh School of Medicine, Pennsylvania 15213, USA.

出版信息

Ann N Y Acad Sci. 1999 Jun 29;877:614-37. doi: 10.1111/j.1749-6632.1999.tb09292.x.

DOI:10.1111/j.1749-6632.1999.tb09292.x
PMID:10415674
Abstract

Functional neuroimaging studies of the anatomical correlates of familial major depressive disorder (MDD) and bipolar disorder (BD) have identified abnormalities of resting blood flow (BF) and glucose metabolism in depression in the amygdala and the orbital and medial prefrontal cortical (PFC) areas that are extensively connected with the amygdala. The amygdala metabolism in MDD and BD is positively correlated with both depression severity and "stressed" plasma cortisol concentrations measured during scanning. During antidepressant drug treatment, the mean amygdala metabolism decreases in treatment responders, and the persistence of elevated amygdala metabolism during remission is associated with a high risk for the development of depressive relapse. The orbital C metabolism is also abnormally elevated during depression, but is negatively correlated with both depression severity and amygdala metabolism, suggesting that this structure may be activated as a compensatory mechanism to modulate amygdala activity or amygdala-driven emotional responses. The posterior orbital C and anterior cingulate C ventral to the genu of the corpus callosum (subgenual PFC) have more recently been shown in morphometric MRI and/or post mortem histopathological studies to have reduced grey matter volume and reduced glial cell numbers (with no equivalent loss of neurons) in familial MDD and BD. These data suggest a neural model in which dysfunction of limbic PFC structures impairs the modulation of the amygdala, leading to abnormal processing of emotional stimuli. Antidepressant drugs may compensate for this dysfunction by inhibiting pathological limbic activity.

摘要

对家族性重度抑郁症(MDD)和双相情感障碍(BD)的解剖学关联进行的功能性神经影像学研究发现,杏仁核以及与杏仁核广泛相连的眶额和内侧前额叶皮质(PFC)区域在抑郁症患者中存在静息血流(BF)和葡萄糖代谢异常。MDD和BD患者的杏仁核代谢与抑郁严重程度以及扫描期间测量的“应激”血浆皮质醇浓度均呈正相关。在抗抑郁药物治疗期间,治疗有反应者的杏仁核平均代谢降低,缓解期杏仁核代谢持续升高与抑郁复发的高风险相关。抑郁症患者的眶额皮质代谢在抑郁期间也异常升高,但与抑郁严重程度和杏仁核代谢均呈负相关,这表明该结构可能作为一种补偿机制被激活,以调节杏仁核活动或杏仁核驱动的情绪反应。最近,在形态计量MRI和/或死后组织病理学研究中发现,家族性MDD和BD患者胼胝体膝部下方的眶额皮质后部和前扣带回皮质(膝下PFC)灰质体积减少,胶质细胞数量减少(神经元无同等程度损失)。这些数据提示了一种神经模型,即边缘系统PFC结构功能障碍会损害对杏仁核的调节,导致情绪刺激的异常处理。抗抑郁药物可能通过抑制病理性边缘系统活动来补偿这种功能障碍。

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