Patten S B
Department of Community Health Sciences and Department of Psychiatry,University of Calgary,Mathison Centre for Research & Education in Mental Health,Hotchkiss Brain Institute,University of Calgary,3rd Floor TRW Building,3280 Hospital Drive NW,Calgary,AB,CanadaT2N 4Z6.
Epidemiol Psychiatr Sci. 2015 Aug;24(4):303-8. doi: 10.1017/S2045796015000153. Epub 2015 Feb 16.
The aetiology of depression is not fully understood, which allows many different perspectives on aetiology to be adopted. Researchers and clinicians may be attracted to concepts of aetiology that parallel other diagnoses with which they are familiar. Such parallels may assume the role of informal models or metaphors for depressive disorders. They may even function as informal scientific theories of aetiology, energising research activities by guiding hypothesis generation and organising new knowledge. Parallels between different types of disease may ultimately prove valuable as frameworks supporting the emergence and maturation of new knowledge. However, such models may be counterproductive if their basis, which is likely to lay at least partially in analogy, is unacknowledged or overlooked. This could cause such models to appear more compelling than they really are. Listing examples of situations in which models of depression may arise from, or be strengthened by, parallels to other familiar conditions may increase the accessibility of such models either to criticism or support. However, such a list has not yet appeared in the literature. The present paper was written with the modest goal of stating several examples of models or metaphors for depression.
This paper adopted narrative review methods. The intention was not to produce a comprehensive list of such ideas, but rather to identify prominent examples of ways of thinking about depression that may have been invigorated as a result parallels with other types of disease.
Eight possible models are identified: depressive disorders as chemical imbalances (e.g., a presumed or theoretical imbalance of normally balanced neurotransmission in the brain), degenerative conditions (e.g., a brain disease characterised by atrophy of specified brain structures), toxicological syndromes (a result of exposure to a noxious psychological environment), injuries (e.g., externally induced brain damage related to stress), deficiency states (e.g., a serotonin deficiency), an obsolete category (e.g., similar to obsolete terms such as 'consumption' or 'dropsy'), medical mysteries (e.g., a condition poised for a paradigm-shifting breakthrough) or evolutionary vestiges (residual components of once adaptive mechanisms have become maladaptive in modern environments).
Conceptualisation of depressive disorders may be partially shaped by familiar disease concepts. Analogies of this sort may ultimately be productive (e.g., through generating hypotheses by analogy) or destructive (e.g., by structuring knowledge in incorrect, but intellectually seductive, ways).
抑郁症的病因尚未完全明确,这使得人们可以从许多不同的角度来探讨病因。研究人员和临床医生可能会被与他们熟悉的其他诊断相似的病因概念所吸引。这种相似性可能会充当抑郁症非正式的模型或隐喻。它们甚至可能作为非正式的病因科学理论发挥作用,通过指导假设生成和组织新知识来推动研究活动。不同类型疾病之间的相似性最终可能被证明是支持新知识出现和成熟的有价值框架。然而,如果这些模型的基础(很可能至少部分基于类比)未被承认或被忽视,那么这些模型可能会适得其反。这可能会使这些模型看起来比实际更有说服力。列举抑郁症模型可能源于与其他熟悉病症的相似性或因这种相似性而得到强化的情况示例,可能会使这些模型更容易受到批评或支持。然而,这样的列表尚未出现在文献中。本文的撰写目的较为 modest,即陈述几个抑郁症模型或隐喻的示例。
本文采用叙述性综述方法。目的不是列出此类观点的完整清单,而是识别因与其他类型疾病的相似性而可能得到激发的关于抑郁症的突出思维方式示例。
确定了八种可能的模型:抑郁症是化学失衡(例如,大脑中正常平衡的神经传递假定或理论上的失衡)、退行性疾病(例如,以特定脑结构萎缩为特征的脑部疾病)、毒理学综合征(接触有害心理环境的结果)、损伤(例如,与压力相关的外部诱发脑损伤)、缺乏状态(例如,血清素缺乏)、过时类别(例如,类似于“痨病”或“水肿”等过时术语)、医学谜团(例如,一种有望实现范式转变突破的病症)或进化遗迹(曾经适应性机制的残余成分在现代环境中已变得适应不良)。
抑郁症的概念化可能部分受到熟悉的疾病概念的影响。这种类比最终可能是有成效的(例如,通过类比生成假设)或具有破坏性的(例如,以不正确但在智力上具有吸引力的方式构建知识)。