Limbic-cortical dysregulation: a proposed model of depression.
Limbic-cortical dysregulation: a proposed model of depression.
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DOI：
10.1176/jnp.9.3.471
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发表时间：
1997
期刊：
影响因子：
--
通讯作者：
H. Mayberg
中科院分区：
文献类型：
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作者：
H. Mayberg
抑郁症的工作模式涉及失败的协调互动的分布式网络的边缘皮质通路的建议。特发性抑郁症患者局部葡萄糖代谢的静息状态模式、抗抑郁药治疗引起的代谢变化以及健康受试者因悲伤引起的血流变化被用来检验和完善这一假设。背侧新皮质减少和腹侧边缘增加的特点都健康的悲伤和抑郁症;并发抑制过度活跃的边缘区和正常化的功能减退的背侧皮质网站的特点疾病缓解。正常功能的喙前扣带回，其直接连接到这些背侧和腹侧地区，被假定为额外需要观察到的相互代偿性变化，因为在这个地区的预处理代谢唯一预测抗抑郁药治疗反应。该模型提供了一个适应性强的框架，以促进临床影像学研究结果与互补的神经解剖学，神经化学和电生理学研究在情感障碍的发病机制的调查持续整合。
A working model of depression implicating failure of the coordinated interactions of a distributed network of limbic-cortical pathways is proposed. Resting state patterns of regional glucose metabolism in idiopathic depressed patients, changes in metabolism with antidepressant treatment, and blood flow changes with induced sadness in healthy subjects were used to test and refine this hypothesis. Dorsal neocortical decreases and ventral paralimbic increases characterize both healthy sadness and depressive illness; concurrent inhibition of overactive paralimbic regions and normalization of hypofunctioning dorsal cortical sites characterize disease remission. Normal functioning of the rostral anterior cingulate, with its direct connections to these dorsal and ventral areas, is postulated to be additionally required for the observed reciprocal compensatory changes, since pretreatment metabolism in this region uniquely predicts antidepressant treatment response. This model is offered as an adaptable framework to facilitate continued integration of clinical imaging findings with complementary neuroanatomical, neurochemical, and electrophysiological studies in the investigation of the pathogenesis of affective disorders.