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[应激理论与躯体化过程]

[Stress theories and the somatization process].

作者信息

Dantzer R

机构信息

Neurobiologie integrative, INSERM U394, Bordeaux.

出版信息

Encephale. 1995 Dec;21 Spec No 7:3-9.

PMID:8929672
Abstract

Stress theories aim at understanding pathophysiology of psychosomatic disorders. The first stress theories have been inspired by the principles of homeostasis. They view the response to stressors as a quasi reflex reaction which aims at normalizing disturbed homeostasis. More modern stress theories emphasize the intermediate role of cognitive and behavioural processes in the determinism of neuroendocrine and neurovegetative responses to stressors. Active attempts to control the situation are associated with activation of the sympathetic and adrenal medullary system whereas loss of control is associated with activation of the hypothalamic-pituitary-adrenal axis. Since the functional consequences of the activation of each of these physiological systems are not the same, the risk factors corresponding to each coping strategy are not the same. Whatever their details, physiological and psychobiological stress theories all emphasize the influence of psychic factors on bodily functions. However, mental states do not function independently of bodily functions. In the case of the influences of stress on immunity for instance, it has been shown that these influences represent the counterpart of feedback regulatory mechanisms in which the ability of the brain to regulate immune responses depends on the capacity of the immune system to influence brain functions. Activation of the immune system during infection or inflammation is accompanied by profound metabolic, neuroendocrine and behavioural changes which are mediated by the effects of immune products known as cytokines on brain cell targets. In view of the reciprocal relationships between peripheral organic systems and the brain, a purely psychosomatic view, from the psyche to the soma, is therefore no longer tenable. In addition, biological accounts of somatization processes run into the risk of minimizing the importance of perception and representation of somatic symptoms. Amplification of somatic symptoms is a common feature of neuroticism or negative affectivity and it bears no relationship with objective pathology. In order to understand somatization processes, there is therefore a need to study how the brain processes information it receives from the body and the way this information competes with information from the external environment.

摘要

应激理论旨在理解心身疾病的病理生理学。最早的应激理论受到内稳态原理的启发。它们将对应激源的反应视为一种准反射反应,目的是使紊乱的内稳态恢复正常。更现代的应激理论强调认知和行为过程在对应激源的神经内分泌和神经植物性反应的决定作用中的中间作用。积极尝试控制局面与交感神经和肾上腺髓质系统的激活有关,而失去控制则与下丘脑 - 垂体 - 肾上腺轴的激活有关。由于这些生理系统中每一个激活的功能后果并不相同,与每种应对策略相对应的风险因素也不相同。无论其细节如何,生理和心理生物学应激理论都强调心理因素对身体功能的影响。然而,心理状态并非独立于身体功能发挥作用。例如,在应激对免疫的影响方面,已经表明这些影响代表了反馈调节机制的对应物,其中大脑调节免疫反应的能力取决于免疫系统影响大脑功能的能力。感染或炎症期间免疫系统的激活伴随着深刻的代谢、神经内分泌和行为变化,这些变化是由被称为细胞因子的免疫产物对脑细胞靶点的作用介导的。鉴于外周有机系统与大脑之间的相互关系,因此从心理到身体的纯粹心身观点不再站得住脚。此外,躯体化过程的生物学解释存在将躯体症状的感知和表征的重要性最小化的风险。躯体症状的放大是神经质或消极情感的常见特征,并且与客观病理学无关。因此,为了理解躯体化过程,有必要研究大脑如何处理从身体接收到的信息以及这种信息与来自外部环境的信息竞争的方式。

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