Hinojosa Cecilia A, van Rooij Sanne J H, Fani Negar, Ellis Robyn A, Harnett Nathaniel G, Lebois Lauren A M, Ely Timothy D, Jovanovic Tanja, Murty Vishnu P, House Stacey L, Beaudoin Francesca L, An Xinming, Neylan Thomas C, Clifford Gari D, Linnstaedt Sarah D, Germine Laura T, Rauch Scott L, Haran John P, Storrow Alan B, Lewandowski Christopher, Musey Paul I, Hendry Phyllis L, Sheikh Sophia, Jones Christopher W, Punches Brittany E, Hudak Lauren A, Pascual Jose L, Seamon Mark J, Harris Erica, Pearson Claire, Peak David A, Merchant Roland C, Domeier Robert M, Rathlev Niels K, O'Neil Brian J, Sergot Paulina, Bruce Steven E, Pizzagalli Diego A, Sheridan John F, Harte Steven E, Koenen Karestan C, Kessler Ronald C, McLean Samuel A, Ressler Kerry J, Stevens Jennifer S
Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, Georgia.
Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, Georgia.
Biol Psychiatry Cogn Neurosci Neuroimaging. 2025 Mar;10(3):314-323. doi: 10.1016/j.bpsc.2024.09.015. Epub 2024 Oct 9.
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 posttrauma in humans. Neuroimaging markers may be particularly useful because they can provide insight into the mechanisms that may make an individual vulnerable to developing trauma-related psychopathologies. In this study, we aimed to identify reward-related neural correlates associated with changes in alcohol use after trauma exposure.
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 posttrauma relative to pretrauma 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 were assessed 2 weeks posttrauma using functional magnetic resonance imaging during a monetary reward task using region of interest and whole-brain voxelwise analyses.
Greater increase in alcohol use from pretrauma to 8 weeks posttrauma was predicted by 1) greater ventral tegmental area, 2) greater cerebellum activation during gain > loss trials measured 2 weeks posttrauma, and 3) greater seed-based functional connectivity between the ventral tegmental area and lateral occipital cortex and precuneus.
Altered ventral tegmental area activation and functional connectivity early posttrauma may be associated with reward seeking and processing, thereby contributing to greater alcohol use posttrauma. These data provide novel evidence of neural correlates that underlie increased alcohol use early posttrauma that may be targeted via early interventions to prevent the development of maladaptive alcohol use.
创伤是导致适应不良性饮酒的一个风险因素。临床前研究表明，应激会改变中脑和纹状体奖赏及动机信号的处理过程。然而，关于创伤后人类奖赏相关神经回路改变的研究却很少。神经影像标志物可能特别有用，因为它们可以深入了解可能使个体易患创伤相关精神病理学的机制。在本研究中，我们旨在确定与创伤暴露后饮酒变化相关的奖赏相关神经关联。
从美国急诊科招募参与者进行AURORA研究（n = 286；178名女性）。根据PhenX工具包酒精30天量和频率测量法，将创伤后8周相对于创伤前饮酒使用的创伤相关变化量化为30天总饮酒量的变化。在创伤后2周，使用功能磁共振成像，通过感兴趣区域和全脑体素分析，在金钱奖赏任务期间评估奖赏相关神经回路的激活和功能连接。
创伤前到创伤后8周饮酒量增加幅度更大可由以下因素预测：1）腹侧被盖区更大；2）创伤后2周测量的收益>损失试验期间小脑激活更强；3）腹侧被盖区与枕外侧皮质和楔前叶之间基于种子的功能连接更强。
创伤后早期腹侧被盖区激活和功能连接的改变可能与奖赏寻求和处理有关，从而导致创伤后饮酒量增加。这些数据为创伤后早期饮酒量增加背后的神经关联提供了新的证据，可通过早期干预来针对这些关联，以预防适应不良性饮酒的发展。
