Department of Psychiatry and Behavioral Sciences, Duke University School of Medicine, Box 102848, Durham, NC, 27708, USA.
Brain Imaging and Analysis Center, Duke University, Durham, NC, USA.
BMC Neurosci. 2021 Aug 20;22(1):51. doi: 10.1186/s12868-021-00654-z.
Delay discounting has been proposed as a behavioral marker of substance use disorders. Innovative analytic approaches that integrate information from multiple neuroimaging modalities can provide new insights into the complex effects of drug use on the brain. This study implemented a supervised multimodal fusion approach to reveal neural networks associated with delay discounting that distinguish persons with and without cocaine use disorder (CUD).
Adults with (n = 35) and without (n = 37) CUD completed a magnetic resonance imaging (MRI) scan to acquire high-resolution anatomical, resting-state functional, and diffusion-weighted images. Pre-computed features from each data modality included whole-brain voxel-wise maps for gray matter volume, fractional anisotropy, and regional homogeneity, respectively. With delay discounting as the reference, multimodal canonical component analysis plus joint independent component analysis was used to identify co-alterations in brain structure and function.
The sample was 58% male and 78% African-American. As expected, participants with CUD had higher delay discounting compared to those without CUD. One joint component was identified that correlated with delay discounting across all modalities, involving regions in the thalamus, dorsal striatum, frontopolar cortex, occipital lobe, and corpus callosum. The components were negatively correlated with delay discounting, such that weaker loadings were associated with higher discounting. The component loadings were lower in persons with CUD, meaning the component was expressed less strongly.
Our findings reveal structural and functional co-alterations linked to delay discounting, particularly in brain regions involved in reward salience, executive control, and visual attention and connecting white matter tracts. Importantly, these multimodal networks were weaker in persons with CUD, indicating less cognitive control that may contribute to impulsive behaviors.
延迟折扣已被提出作为物质使用障碍的行为标志物。整合来自多种神经影像学模式的信息的创新分析方法可以为研究药物使用对大脑的复杂影响提供新的见解。本研究实施了一种有监督的多模态融合方法,以揭示区分有无可卡因使用障碍(CUD)的个体的与延迟折扣相关的神经网络。
有(n=35)和无(n=37)CUD 的成年人完成了磁共振成像(MRI)扫描,以获取高分辨率解剖、静息态功能和弥散加权图像。每个数据模态的预计算特征分别包括全脑体素水平的灰质体积、各向异性分数和局部一致性图。以延迟折扣为参考,多模态典型成分分析加联合独立成分分析用于识别大脑结构和功能的共同改变。
该样本中 58%为男性,78%为非裔美国人。正如预期的那样,CUD 参与者的延迟折扣率高于无 CUD 参与者。确定了一个与所有模态的延迟折扣相关的联合成分,涉及丘脑、背侧纹状体、额极皮质、枕叶和胼胝体的区域。该成分与延迟折扣呈负相关,即较弱的负荷与较高的折扣相关。CUD 患者的成分负荷较低,这意味着该成分的表达较弱。
我们的研究结果揭示了与延迟折扣相关的结构和功能共同改变,特别是在涉及奖励突显、执行控制和视觉注意力以及连接白质束的大脑区域。重要的是,这些多模态网络在 CUD 患者中较弱,表明认知控制能力较弱,这可能导致冲动行为。