Constantino-Pettit Anna, Gilbert Kirsten, Boone Kiran, Luking Katherine, Geselowitz Benjamin, Tillman Rebecca, Whalen Diana, Luby Joan, Barch Deanna M, Vogel Alecia
Department of Psychiatry, Washington University in St. Louis, School of Medicine, St. Louis, Missouri.
Department of Psychiatry, Washington University in St. Louis, School of Medicine, St. Louis, Missouri.
Biol Psychiatry Cogn Neurosci Neuroimaging. 2025 Jan 28. doi: 10.1016/j.bpsc.2025.01.010.
The current understanding of the neural correlates of borderline personality disorder (BPD) is limited, but some evidence suggests that alterations in limbic structures play a role in adult BPD. The developmental course of structural neural differences in BPD is unknown. Whether there is specificity for structural alterations in BPD compared to other psychiatric presentations, such as major depressive disorder (MDD), remains unexplored. In the current study, we examined childhood trajectories of 2 limbic regions that have been implicated in BPD, hippocampal and amygdala volume, as they relate to adolescent BPD symptoms compared to MDD symptoms.
Participants (n = 175; 85 [48.6%] female) were from a 17-year longitudinal study of preschool depression. Participants completed up to 5 magnetic resonance imaging scans from late childhood through adolescence. General linear models were used to examine the relationship between gray matter volume intercepts/slopes and BPD symptoms to understand the influence of the developmental trajectory of brain regions on BPD. Separate models were used to examine the relationship between MDD symptoms and volume intercepts to assess diagnostic specificity.
Lower childhood amygdala volume (intercept; age 13 centered) across scans was associated with higher adolescent BPD symptoms (β = -0.25, adjusted p = .015). There was no relationship between the slope of amygdala volume and BPD symptoms. There was no relationship between hippocampal volume and BPD or any relationship between amygdala or hippocampal volume and MDD symptoms during adolescence.
Our findings add evidence that supports the role of alterations in amygdala structure in BPD development. Decreased amygdala volume as early as age 13 may be an early indicator of the development of BPD during adolescence.
目前对边缘型人格障碍(BPD)神经关联的理解有限,但一些证据表明边缘系统结构的改变在成人BPD中起作用。BPD中结构性神经差异的发展过程尚不清楚。与其他精神疾病表现(如重度抑郁症(MDD))相比,BPD的结构改变是否具有特异性仍未得到探索。在本研究中,我们研究了与BPD相关的两个边缘区域(海马体和杏仁核体积)的儿童期轨迹,以及它们与青少年BPD症状和MDD症状的关系。
参与者(n = 175;85名[48.6%]女性)来自一项针对学龄前抑郁症的17年纵向研究。参与者从儿童晚期到青少年期完成了多达5次磁共振成像扫描。使用一般线性模型来检验灰质体积截距/斜率与BPD症状之间的关系,以了解脑区发育轨迹对BPD的影响。使用单独的模型来检验MDD症状与体积截距之间的关系,以评估诊断特异性。
在各次扫描中,儿童期杏仁核体积较低(截距;以13岁为中心)与青少年期较高的BPD症状相关(β = -0.25,校正p = .015)。杏仁核体积斜率与BPD症状之间没有关系。海马体体积与BPD之间没有关系,在青少年期,杏仁核或海马体体积与MDD症状之间也没有任何关系。
我们的研究结果进一步证明了杏仁核结构改变在BPD发展中的作用。早在13岁时杏仁核体积减小可能是青少年期BPD发展的早期指标。