Understanding the interface between opioid use disorder (OUD) and post-traumatic stress disorder (PTSD) is challenging. By use of a dimensional framework, such as research domain criteria, convergent and targetable neurobiological processes in OUD–PTSD comorbidity can be identified. We hypothesise that, in OUD–PTSD, circuitry that is implicated in two research domain criteria systems (ie, negative valence and cognitive control) underpins dysregulation of incentive salience, negative emotionality, and executive function. We also propose that the OUD–PTSD state might be systematically investigated with approaches outlined within a neuroclinical assessment framework for addictions and PTSD. Our dimensional analysis of the OUD–PTSD state shows how first-line therapeutic approaches (ie, partial μ-type opioid receptor [MOR1] agonism) modulate overlapping neurobiological and clinical features and also provides mechanistic rationale for evaluating polytherapeutic strategies (ie, partial MOR1 agonism, κ-type opioid receptor [KOR1] antagonism, and α-2A adrenergic receptor [ADRA2A] agonism). A combination of these therapeutic mechanisms is projected to facilitate recovery in patients with OUD–PTSD by mitigating negative valence states and enhancing executive control.

了解阿片类药物使用障碍 (OUD) 和创伤后应激障碍 (PTSD) 之间的关系具有挑战性。通过使用维度框架，例如研究领域标准，可以识别 OUD-PTSD 合并症中的收敛和可靶向神经生物学过程。我们假设，在 OUD-PTSD 中，涉及两个研究领域标准系统（即负效价和认知控制）的电路支持激励显着性、负性情绪和执行功能的失调。我们还建议，可以使用成瘾和 PTSD 的神经临床评估框架内概述的方法系统地研究 OUD-PTSD 状态。我们对 OUD-PTSD 状态的维度分析显示了一线治疗方法（即，部分 μ 型阿片受体 [MOR1] 激动剂）调节重叠的神经生物学和临床特征，并为评估多治疗策略（即部分 MOR1 激动剂、κ 型阿片受体 [KOR1] 拮抗剂和 α-2A 肾上腺素能受体 [ ADRA2A] 激动）。预计这些治疗机制的组合将通过减轻负价态和增强执行控制来促进 OUD-PTSD 患者的康复。