Biopsychosocial model in depression revisited
Biopsychosocial model in depression revisited
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DOI：
10.1016/j.mehy.2006.02.049
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发表时间：
2007-01-01
影响因子：
4.7
通讯作者：
Aguirre, Iratxe
中科院分区：
文献类型：
--
作者：
Garcia-Toro, Mauro;Aguirre, Iratxe
关于精神障碍有两种基本的病因学观点：生物医学和心理社会。生物心理社会模型声称以科学的方式整合这两种观点，表明它们的相互关联和相互依赖。为此，它使用了一个系统的概念框架，利用它提供的可能性为不同的系统建立一般原则，独立于它们的物理、生物或社会学性质。近年来，借鉴系统理论，动态非线性系统的理论不断发展，适用于大量紧密互连的元素（也称为复杂系统）的网络，例如心灵或大脑。我们相信，这个修订后的系统概念框架可以带来适用于抑郁症的综合思想，例如我们在本文中使用的“结合功能障碍”概念。据此，抑郁症的脆弱性或易感性可能与激活和抑制相互作用之间的不平衡（心理层面的某些认知和情绪之间，以及大脑层面的某些神经元群之间）之间的不平衡有关。诱发因素意味着这种认知和情绪模式或神经元系统的激活水平增加。当压力超过脆弱性阈值时，认知和情绪之间（以及神经元组之间）会出现过度的正反馈，而抑制控制不足以缓解它，这意味着不同激活水平领域中的精神/大脑分离。因此，大脑和精神激活模式的产生和消解将不再具有允许与环境进行最佳相互作用的活力和灵活性（“结合功能障碍”）。因此，我们的假设是，抑郁症患者在大脑水平上会在确定的位置遭受神经支配的功能分离（一些严格过度活跃，另一些严格低活跃），这将与其他精神障碍中发现的组合不同。在心理层面上，这可能与几个认知情感领域的功能分离有关。有些对应于过度激活的“抑郁”认知和情绪模式，因此频繁、侵入性和重复地侵入意识；与此同时，还有其他一些不活跃的情绪和认知，它们无法变得强大到足以避免随之而来的与环境沟通的扭曲。 (c) 2006 Elsevier Ltd. 保留所有权利。
There are two fundamental etiological perspectives about mental disorders; biomedical and psychosocial. The biopsychosocial model has claimed to integrate these two perspectives in a scientific way, signalling their interconnection and interdependence. To that end, it used a systemic conceptual framework, taking advantage of the possibilities which it offers to establish general principles for diverse systems, independently of their physical, biological or sociological nature. In recent years, drawing on the theory of systems, theories have been developing of the dynamic non-linear systems, applicable to networks of a large quantity of densely interconnected elements (also called complex systems), like the mind or the brain. We believe that this revised systemic conceptual framework can bring integrative ideas to apply to Depression, such as the "binding dysfunction" concept we use in this article. According to this, vulnerability or predisposition to Depression would be associated with the imbalance between activating and inhibiting interactions (between some cognitions and emotions at a mental level, and between certain neuronal groups at a cerebral level). Precipitating factors would imply the increase of the activation level over this pattern of cognitions and emotions, or over those neuronal systems. When stress goes beyond the vulnerability threshold an excessive positive feedback between cognitions and emotions would appear (and between groups of neurons) with insufficient inhibitory control to mitigate it, which would imply a mental/cerebral dissociation in dominions of different level of activation. As a consequence, the generation and dissolution of patterns of cerebral and mental activation will no Longer have the dynamism and flexibility that permits an optimal interaction with the environment ("binding dysfunction"). Therefore, our hypothesis is that the person with Depression will suffer at a cerebral level a functional dissociation in neural dominions (some rigidly hyperactive and others rigidly hypoactive) in determined locations, which would be a different combination from those found in other mental disorders. At a mental level, this would correlate with a functional dissociation in several cognitive-emotive dominions; some corresponds to over activated patterns of "depressive" cognitions and emotions that for that reason invade the consciousness frequently, intrusively and repetitively; meanwhile there are other alternative hypoactive emotions and cognitions that do not manage to become powerful enough to avoid the consequent distortion in the communication with the environment. (c) 2006 Elsevier Ltd. All rights reserved.