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从正常恐惧到病理性焦虑。

From normal fear to pathological anxiety.

作者信息

Rosen J B, Schulkin J

机构信息

Department of Psychology, University of Delaware, Newark 19716, USA.

出版信息

Psychol Rev. 1998 Apr;105(2):325-50. doi: 10.1037/0033-295x.105.2.325.

DOI:10.1037/0033-295x.105.2.325
PMID:9577241
Abstract

In this article the authors address how pathological anxiety may develop from adaptive fear states. Fear responses (e.g., freezing, startle, heart rate and blood pressure changes, and increased vigilance) are functionally adaptive behavioral and perceptual responses elicited during danger to facilitate appropriate defensive responses that can reduce danger or injury (e.g., escape and avoidance). Fear is a central motive state of action tendencies subserved by fear circuits, with the amygdala playing a central role. Pathological anxiety is conceptualized as an exaggerated fear state in which hyperexcitability of fear circuits that include the amygdala and extended amygdala (i.e., bed nucleus of the stria terminalis) is expressed as hypervigilance and increased behavioral responsivity to fearful stimuli. Reduced thresholds for activation and hyperexcitability in fear circuits develop through sensitization- or kindling-like processes that involve neuropeptides, hormones, and other proteins. Hyperexcitability in fear circuits is expressed as pathological anxiety that is manifested in the various anxiety disorders.

摘要

在本文中,作者探讨了病理性焦虑如何从适应性恐惧状态发展而来。恐惧反应(例如,僵住、惊吓反应、心率和血压变化以及警觉性提高)是在危险期间引发的功能性适应性行为和感知反应,以促进能够减少危险或伤害的适当防御反应(例如,逃跑和回避)。恐惧是由恐惧回路支持的行动倾向的核心动机状态,杏仁核起着核心作用。病理性焦虑被概念化为一种过度的恐惧状态,其中包括杏仁核和扩展杏仁核(即终纹床核)的恐惧回路的过度兴奋表现为过度警觉和对恐惧刺激的行为反应性增加。恐惧回路中激活阈值的降低和过度兴奋是通过涉及神经肽、激素和其他蛋白质的敏化或点燃样过程发展而来的。恐惧回路的过度兴奋表现为病理性焦虑,这在各种焦虑症中都有体现。

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