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社交焦虑障碍的神经生物学:恐惧与焦虑的相关性

The neurobiology of social anxiety disorder: the relevance of fear and anxiety.

作者信息

Marcin M S, Nemeroff C B

机构信息

Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, GA 30322, USA.

出版信息

Acta Psychiatr Scand Suppl. 2003(417):51-64. doi: 10.1034/j.1600-0447.108.s417.4.x.

Abstract

OBJECTIVE

Social anxiety disorder (SAD) is a ubiquitous anxiety disorder. Despite being the third most common psychiatric disorder, little is known about the interaction between genetic predisposition and environmental factors in the development of SAD. The available literature on SAD has been compared with data on the genetics and environmental impact on the phenotypic expression of fear and anxiety, and its implicated neurobiology, in order to explore the neurobiology of SAD as understood through the neurochemical dysregulation expressed in fear and anxiety.

METHOD

A systematic review of the literature was employed for the years from 1966 to 2001.

RESULTS

SAD does indeed have much overlap with fear and anxiety. This is best demonstrated by the interactions of the noradrenergic and serotonergic systems with each other and the hypothalamic-pituitary-adrenal axis.

CONCLUSION

SAD may well be understood as one potential outcome for predisposed individuals who are exposed to the proverbial 'second hit', or environmental insult, in childhood. Behavioral inhibition may be an early expression of this predisposition, with natural progression to SAD occurring via a disruption of neurochemical homeostasis. Through animal and human data it has become evident that fear and anxiety have shared, as well as distinct, neurochemical and neuroanatomical pathways. These similarities are expressed as symptoms and objective signs that are common to many individuals with social anxiety disorder.

摘要

目的

社交焦虑障碍(SAD)是一种普遍存在的焦虑症。尽管它是第三大常见的精神疾病,但对于遗传易感性与环境因素在社交焦虑障碍发展过程中的相互作用,人们知之甚少。已将关于社交焦虑障碍的现有文献与有关遗传和环境对恐惧与焦虑的表型表达及其相关神经生物学影响的数据进行了比较,以便通过恐惧和焦虑中表达的神经化学失调来探索社交焦虑障碍的神经生物学机制。

方法

对1966年至2001年期间的文献进行了系统综述。

结果

社交焦虑障碍确实与恐惧和焦虑有很多重叠之处。去甲肾上腺素能系统和5-羟色胺能系统之间以及下丘脑-垂体-肾上腺轴之间的相互作用最能证明这一点。

结论

社交焦虑障碍很可能被理解为易患个体在童年时期遭受所谓的“二次打击”或环境伤害后的一种潜在结果。行为抑制可能是这种易感性的早期表现,通过神经化学稳态的破坏自然发展为社交焦虑障碍。通过动物和人类数据已经明显看出,恐惧和焦虑既有共同的,也有不同的神经化学和神经解剖学途径。这些相似之处表现为许多社交焦虑障碍患者共有的症状和客观体征。

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