Neuroimaging studies of mood disorders
Neuroimaging studies of mood disorders
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DOI：
10.1016/s0006-3223(00)01020-9
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发表时间：
2000-10-15
影响因子：
10.6
通讯作者：
Drevets, WC
中科院分区：
文献类型：
--
作者：
Drevets, WC
对重度抑郁症的神经成像研究发现，在眼眶和前额叶内侧皮质、杏仁核以及纹状体和丘脑的相关部分的多个区域存在神经生理异常。这些异常中的一些似乎与情绪状态有关，位于正常和其他病理性情绪状态下脑血流增加的区域。因此，抑郁症患者和对照受试者之间的这些神经生理学差异可能牵涉到生理活动改变的区域，以调节或响应主要抑郁发作的情绪、行为和认知表现。其他异常在症状缓解后持续存在，并在眼眶和内侧前额叶皮质区域发现，尸检显示原发性情绪障碍的冷血容量减少和组织病理学变化。根据来自人类和/或实验动物的脑图、病变分析和电生理学研究的证据，这些区域似乎调节情绪行为和应激反应。因此，涉及这些区域的功能障碍被认为在抑郁症状的发病机制中发挥了作用。综上所述，这些发现涉及相互关联的神经回路，其中神经传递的病理模式可能导致原发性和继发性情感障碍的情绪、动机、认知和行为表现。生物精神病学2000；48：813-829(C)2000生物精神病学学会。
Neuroimaging studies of major depression have identified neurophysiologic abnormalities in multiple areas of the orbital and medial prefrontal cortex, the amygdala, and related parts of the striatum and thalamus. Some of these abnormalities appear mood state-dependent and are located in regions where cerebral blood flow increases during normal and other pathologic emotional states. These neurophysiologic differences between depressives and control subjects may thus implicate areas where physiologic activity changes to mediate or respond to the emotional, behavioral, and cognitive manifestations of major depressive episodes. Other abnormalities persist following symptom remission, and are found in orbital and medial prefrontal cortex areas where postmortem studies demonstrate reductions in colter volume and histopathologic changes in primary mood disorders. These areas appear to modulate emotional behavior and stress responses, based upon evidence from brain mapping, lesion analysis, and electrophysiologic studies of humans and/or experimental animals. Dysfunction involving these regions is thus hypothesized to play a role in the pathogenesis of depressive symptoms. Taken together, these findings implicate interconnected neural circuits in which pathologic patterns of neurotransmission may result in the emotional, motivational, cognitive, and behavioral manifestations of primary and secondary affective disorders. Biol Psychiatry 2000;48:813-829 (C) 2000 Society of Biological Psychiatry.