Discipline of Psychiatry, School of Medicine and Trinity College Institute of Neuroscience, Integrated Neuroimaging, Trinity Academic Medical Centre (The Adelaide and Meath Hospital, incorporating the National Children's Hospital and St. James's Hospital), Trinity College, Dublin, Ireland.
J Psychiatry Neurosci. 2011 Jan;36(1):15-22. doi: 10.1503/jpn.090186.
In major depressive disorder (MDD), it is unclear to what extent structural brain changes are associated with depressive episodes or represent part of the mechanism by which the risk for illness is mediated. The aim of this study was to investigate whether structural abnormalities are related to risk for the development of MDD.
We compared healthy controls with a positive family history for MDD (HC-FHP), healthy controls with no family history of any psychiatric disease (HC-FHN) and patients with MDD. Groups were age- and sex-matched. We analyzed data from high-resolution magnetic resonance imaging using voxel-based morphometry. We performed small volume corrections for our regions of interest (hippocampus, dorsolateral [DLPFC] and dorsomedial prefrontal cortex [DMPFC], anterior cingulate cortex [ACC] and basal ganglia) using a family-wise error correction (p < 0.05) to control for multiple comparisons.
There were 30 participants in the HC-FHP group, 64 in the HC-FHN group and 33 patients with MDD. The HC-FHP group had smaller right hippocampal and DLPFC grey matter volumes compared with the HC-FHN group, and even smaller right hippocampal volumes compared with patients with MDD. In addition, the HC-FHP group exhibited smaller white matter volumes in the DLPFC and left putamen but also greater volumes in 2 areas of the DMPFC compared with the HC-FHN group. Patients with MDD exhibited smaller volumes in the ACC, DMPFC, DLPFC and the basal ganglia compared with healthy controls.
The retrospective identification of family history might result in a bias toward unidentified participants in the control group at risk for MDD, diminishing the effect size.
Volume reductions in the hippocampus and DLPFC might be associated with a greater risk for MDD. The HC-FHP group had smaller hippocampal volumes compared with patients with MDD, which is suggestive for neuroplastic effects of treatment. The HC-FHP group had not yet experienced a depressive episode and therefore might have been resilient and might have had some protective strategies. Whether resilience is associated with the larger white matter volumes in the DMPFC (e.g., owing to compensatory, neuroplastic remodelling mechanisms) needs to be confirmed in future studies.
在重度抑郁症（MDD）中，尚不清楚结构脑变化与抑郁发作的关系，或者这些变化是否代表了疾病风险中介的机制的一部分。本研究旨在探讨结构异常是否与 MDD 发展的风险有关。
我们比较了有 MDD 阳性家族史的健康对照组（HC-FHP）、无任何精神疾病家族史的健康对照组（HC-FHN）和 MDD 患者。组间进行年龄和性别匹配。我们使用基于体素的形态测量学分析高分辨率磁共振成像数据。我们对感兴趣的区域（海马体、背外侧前额叶皮质[DLPFC]和背内侧前额叶皮质[DMPFC]、前扣带回皮质[ACC]和基底节）进行小体积校正，使用家族性错误校正（p<0.05）控制多重比较。
HC-FHP 组有 30 名参与者，HC-FHN 组有 64 名参与者，MDD 患者组有 33 名参与者。与 HC-FHN 组相比，HC-FHP 组的右侧海马体和 DLPFC 灰质体积较小，与 MDD 患者相比甚至更小。此外，HC-FHP 组的 DLPFC 和左侧壳核的白质体积较小，但 DMPFC 的 2 个区域的体积较大。与健康对照组相比，MDD 患者的 ACC、DMPFC、DLPFC 和基底节的体积较小。
家族史的回顾性识别可能导致对照组中未识别的 MDD 高危参与者的偏倚，从而降低效应大小。
海马体和 DLPFC 的体积减少可能与 MDD 的发病风险增加有关。与 MDD 患者相比，HC-FHP 组的海马体体积较小，这提示治疗有神经可塑性作用。HC-FHP 组尚未经历抑郁发作，因此可能具有弹性，并且可能具有一些保护策略。在未来的研究中，需要确认弹性是否与 DMPFC 较大的白质体积（例如，由于补偿性、神经可塑性重塑机制）有关。
