Reward neurocircuitry predicts longitudinal changes in alcohol use following trauma exposure.

Cecilia A Hinojosa, Sanne J H van Rooij, Negar Fani, Robyn A Ellis, Nathaniel G Harnett, Lauren A M Lebois, Timothy D Ely, Tanja Jovanovic, Vishnu P Murty, Stacey L House, Francesca L Beaudoin, Xinming An, Thomas C Neylan, Gari D Clifford, Sarah D Linnstaedt, Laura T Germine, Scott L Rauch, John P Haran, Alan B Storrow, Christopher Lewandowski, Paul I Musey, Phyllis L Hendry, Sophia Sheikh, Christopher W Jones, Brittany E Punches, Lauren A Hudak, Jose L Pascual, Mark J Seamon, Erica Harris, Claire Pearson, David A Peak, Roland C Merchant, Robert M Domeier, Niels K Rathlev, Brian J O'Neil, Paulina Sergot, Steven E Bruce, Diego A Pizzagalli, John F Sheridan, Steven E Harte, Karestan C Koenen, Ronald C Kessler, Samuel A McLean, Kerry J Ressler, Jennifer S Stevens
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Abstract

Background: Trauma is a risk factor for developing maladaptive alcohol use. Preclinical research has shown that stress alters the processing of midbrain and striatal reward and incentive signals. However, little research has been conducted on alterations in reward-related neurocircuitry post-trauma in humans. Neuroimaging markers may be particularly useful as they can provide insight into the mechanisms that may make an individual vulnerable to developing trauma-related psychopathologies. This study aimed to identify reward-related neural correlates associated with changes in alcohol use after trauma exposure.

Methods: Participants were recruited from U.S. emergency departments for the AURORA study (N=286, 178 female). Trauma-related change in alcohol use at 8 weeks post-trauma relative to pre-trauma was quantified as a change in 30-day total drinking per the PhenX Toolkit Alcohol 30-Day Quantity and Frequency Measure. Reward-related neurocircuitry activation and functional connectivity (FC) were assessed 2 weeks post-trauma using fMRI during a monetary reward task using region of interest and whole-brain voxelwise analyses.

Results: Greater increase in alcohol use from pre-trauma to 8 weeks post-trauma was predicted by (1) greater ventral tegmental area (VTA) and (2) greater cerebellum activation during Gain>Loss trials measured 2 weeks post-trauma and (3) greater seed-based FC between the VTA and lateral occipital cortex and precuneus.

Conclusions: Altered VTA activation and FC early post-trauma may be associated with reward-seeking and processing, contributing to greater alcohol use post-trauma. These data provide novel evidence of neural correlates that underlie increased alcohol use early post-trauma that may be targeted via early interventions to prevent the development of maladaptive alcohol use.

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奖赏神经回路可预测遭受创伤后酒精使用的纵向变化。
背景:精神创伤是酗酒的一个危险因素。临床前研究表明,压力会改变中脑和纹状体奖赏和激励信号的处理。然而,有关人类创伤后奖赏相关神经回路改变的研究却很少。神经影像标记可能特别有用,因为它们可以让人们深入了解可能使人容易患上创伤相关精神病理学的机制。本研究旨在确定与创伤后饮酒变化相关的奖赏相关神经相关性:AURORA研究从美国急诊科招募参与者(286人,178名女性)。根据PhenX工具包酒精30天数量和频率测量法,创伤后8周与创伤前相比,与创伤相关的饮酒变化被量化为30天总饮酒量的变化。利用感兴趣区和全脑体素分析,在金钱奖励任务中使用fMRI对创伤后2周与奖励相关的神经回路激活和功能连接(FC)进行评估:结果:从创伤前到创伤后8周,酒精使用量的增加主要是通过以下因素预测的:(1)创伤后2周测量的腹侧被盖区(VTA)增加;(2)在 "得">"失 "试验中小脑激活增加;(3)VTA与外侧枕叶皮层和楔前皮层之间基于种子的FC增加:结论:创伤后早期VTA激活和FC的改变可能与奖赏寻求和处理有关,从而导致创伤后更多的酒精使用。这些数据为创伤后早期酒精使用增加的神经相关性提供了新的证据,可以通过早期干预来预防适应不良的酒精使用。
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