Motion, emotion and cognition: The melancholia conundrum.

IF 1.7 4区 医学 Q4 PSYCHIATRY
Perminder S Sachdev
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引用次数: 0

Abstract

BackgroundThe status of melancholia remains controversial. Debate has focused on whether it represents a categorically distinct disorder (binary model) or a severe expression within a unitary construct of major depressive disorder. Its defining core has also been disputed, with competing emphasis on affective symptoms, cognitive distortions, or psychomotor disturbance. Proponents of distinctiveness, notably Gordon Parker, have argued that psychomotor disturbance is central to the syndrome.ObjectiveTo critically examine historical and contemporary evidence regarding melancholia's diagnostic status and to consider whether advances in neurobiology can resolve longstanding conceptual debates.MethodThis narrative analysis reviews the evolution of the melancholia construct, clinical and treatment-response data, research on psychomotor disturbance including the CORE measure, and recent findings from genetics, molecular psychiatry, and neuroimaging studies of brain networks implicated in depression.ConclusionPhenomenological and biomarker-based approaches have not conclusively established melancholia as a distinct nosological entity. Emerging findings from circuit neuroscience and multiomic research suggest that patterns of large-scale network dysfunction may underlie the clinical syndrome, but have not yet established a reproducible circuit signature specific to melancholia. A biologically grounded, network-based framework could ultimately clarify the relationship between melancholia, psychomotor disturbance and broader depressive syndromes, moving the field beyond the binary-dimensional impasse.

运动、情感和认知:忧郁症的难题。
抑郁症的地位一直存在争议。争论的焦点是它是否代表了一种截然不同的障碍(二元模型),还是一种重性抑郁症的单一结构中的严重表达。其定义的核心也有争议,竞争的重点是情感症状,认知扭曲,或精神运动障碍。以戈登·帕克(Gordon Parker)为代表的独特性的支持者认为,精神运动障碍是该综合征的核心。目的批判性地研究有关抑郁症诊断地位的历史和当代证据,并考虑神经生物学的进步是否可以解决长期存在的概念争论。方法本文回顾了抑郁症结构的演变、临床和治疗反应数据、包括CORE测量在内的精神运动障碍研究,以及遗传学、分子精神病学和与抑郁症有关的脑网络神经影像学研究的最新发现。结论现象学和基于生物标志物的方法并没有最终确定抑郁症是一个独特的疾病实体。电路神经科学和多组学研究的新发现表明,大规模网络功能障碍的模式可能是临床综合征的基础,但尚未建立一个可重复的神经回路特征特异性的抑郁症。一个以生物学为基础、以网络为基础的框架可能最终阐明抑郁症、精神运动障碍和更广泛的抑郁综合症之间的关系,使该领域超越二元维度的僵局。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Australasian Psychiatry
Australasian Psychiatry 医学-精神病学
CiteScore
2.80
自引率
5.60%
发文量
159
审稿时长
6-12 weeks
期刊介绍: Australasian Psychiatry is the bi-monthly journal of The Royal Australian and New Zealand College of Psychiatrists (RANZCP) that aims to promote the art of psychiatry and its maintenance of excellence in practice. The journal is peer-reviewed and accepts submissions, presented as original research; reviews; descriptions of innovative services; comments on policy, history, politics, economics, training, ethics and the Arts as they relate to mental health and mental health services; statements of opinion and letters. Book reviews are commissioned by the editor. A section of the journal provides information on RANZCP business and related matters.
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