Abstract
BackgroundDelay 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).MethodsAdults 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.ResultsThe 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.ConclusionsOur 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.
Highlights
Cocaine use continues to be a significant global health problem
As substance use progresses to addiction, mesostriatal networks become sensitized to drug cues and desensitized to nondrug rewards [5, 6], while cognitive control networks become hijacked by drug reinforcement [7, 8]
cocaine use disorder (CUD) is associated with deficits in reward-based decision making that are often associated with impulsive behaviors [9], and which may contribute to adverse outcomes, such as infectious disease, criminal behaviors, and violence [10, 11]
Summary
Cocaine use continues to be a significant global health problem. In the United States, an estimated 5.5 million people used cocaine in 2018, and nearly 1 million people had a cocaine use disorder (CUD) [1]. In non-clinical samples, brain morphology has been linked to steeper discounting, including lower cortical and higher subcortical gray matter volume (GMV) [26, 27], reduced white mater integrity in brainstem, association, and commissural tracts [28], and lower white matter connectivity between frontal-striatal regions [29]. These neural underpinnings of delay discounting overlap with functional and structural brain alterations identified in CUD. 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)
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
