Kessler Henrik, Traue Harald, Wiswede Daniel
Universitätsklinik für Psychosomatische Medizin und Psychotherapie, Ulm.
Psychosoc Med. 2011;8:Doc06. doi: 10.3205/psm000075. Epub 2011 Sep 23.
Although remarkable progress has been made in the search for the brain correlates of depression with neuroimaging methods, we still find a heterogeneity of results and lack of consensus. This short commentary proposes a theoretical reason for this situation linking it to the methods of conducting neuroimaging studies of depression and the ways to interpret findings. If we only take one snapshot of the "depressed brain", the brain activity is presumably the result of four interacting components: neural predispositions, depressogenic pathology, changes caused by (chronic) depression, and compensatory brain mechanisms. The four components will be discussed briefly along with arguments why confusion of them might confuse our view of the brain in depression. After a short presentation of promising new longitudinal studies, this commentary gives first hints how we could go beyond snapshots to better understand the brain in depression.
尽管在利用神经影像学方法寻找抑郁症的大脑关联方面已取得显著进展,但我们仍发现结果存在异质性且缺乏共识。这篇简短的评论提出了造成这种情况的一个理论原因,将其与抑郁症神经影像学研究的开展方法以及研究结果的解读方式联系起来。如果我们仅对“抑郁大脑”进行一次快照式观察,大脑活动大概是四个相互作用的成分的结果:神经易感性、致抑郁病理、(慢性)抑郁症引起的变化以及大脑的代偿机制。将简要讨论这四个成分,并阐述为何混淆它们可能会扰乱我们对抑郁症患者大脑的看法。在简短介绍了有前景的新纵向研究之后,这篇评论首次给出了一些提示,说明我们如何能够超越快照式观察,以更好地理解抑郁症患者的大脑。