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Biopsychosocial model in Depression revisited.

机译:抑郁症的生物心理社会模型被重新审视。

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摘要

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.
机译:关于精神障碍有两种基本的病因学观点:生物医学和社会心理。生物社会心理学模型声称以科学的方式整合了这两种观点,表明了它们的相互联系和相互依存。为此,它利用了系统的概念框架,并利用其提供的可能性为各种系统建立了通用的原理,而与它们的物理,生物学或社会学性质无关。近年来,利用系统理论,开发了动态非线性系统的理论,该系统适用于大量密集互连的元素(也称为复杂系统)的网络,例如心灵或大脑。我们认为,经过修订的系统概念框架可以带来适用于抑郁症的综合性思想,例如我们在本文中使用的“约束功能障碍”概念。据此,抑郁症的易感性或易感性将与激活和抑制相互作用之间的不平衡相关联(在心理水平上某些认知和情感之间,在大脑水平上某些神经元组之间)。沉淀因素将暗示激活水平在这种认知和情绪模式下或在那些神经元系统上增加。当压力超过脆弱性阈值时,将在认知和情绪之间(以及在神经元组之间)出现过度的积极反馈,而抑制控制不足以减轻压力,这意味着不同激活水平的大脑/大脑会分离。结果,大脑和精神激活模式的产生和消散将不再具有允许与环境最佳相互作用的动力和灵活性(“结合功能障碍”)。因此,我们的假设是,抑郁症患者在确定的位置会在脑部遭受神经支配的功能性分离(某些功能亢进而某些功能亢进),这与其他精神疾病的组合不同。在精神层面上,这将与几个认知情感领域的功能分离相关。其中一些与过度激活的“抑郁”认知和情绪模式相对应,因此,该频率经常,侵入性和重复地侵入意识。同时,还有其他无法替代的过动情绪和认知,这些情绪和认知无法变得足够强大,无法避免与环境沟通的结果扭曲。

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