In the past decade, there has been an increasing awareness that traumatic brain injury (TBI) and concussion substantially increase the risk for developing psychiatric disorders. Even mild TBI increases the risk for depression and anxiety disorders such as posttraumatic stress disorder by two- to threefold, predisposing patients to further functional impairment. This strong epidemiological link supports examination of potential mechanisms driving neuropsychiatric symptom development after TBI. One potential mechanism for increased neuropsychiatric symptoms after TBI is via inflammatory processes, as central nervous system inflammation can last years after initial injury. There is emerging preliminary evidence that TBI patients with posttraumatic stress disorder or depression exhibit increased central and peripheral inflammatory markers compared with TBI patients without these comorbidities. Growing evidence has demonstrated that immune signaling in animals plays an integral role in depressive- and anxiety-like behaviors after severe stress or brain injury. In this review, we will 1) discuss current evidence for chronic inflammation after TBI in the development of neuropsychiatric symptoms, 2) highlight potential microglial activation and cytokine signaling contributions, and 3) discuss potential promise and pitfalls for immune-targeted interventions and biomarker strategies to identify and treat TBI patients with immune-related neuropsychiatric symptoms.

在过去十年中，人们越来越意识到创伤性脑损伤 (TBI) 和脑震荡会大大增加患精神疾病的风险。即使是轻微的 TBI 也会使患抑郁症和焦虑症（例如创伤后应激障碍）的风险增加两到三倍，使患者容易出现进一步的功能障碍。这种强有力的流行病学联系支持检查 TBI 后驱动神经精神症状发展的潜在机制。TBI 后神经精神症状增加的一个潜在机制是通过炎症过程，因为中枢神经系统炎症可以在初始损伤后持续数年。有新的初步证据表明，与没有这些合并症的 TBI 患者相比，患有创伤后应激障碍或抑郁症的 TBI 患者表现出更多的中枢和外周炎症标志物。越来越多的证据表明，动物的免疫信号在严重压力或脑损伤后的抑郁和焦虑样行为中起着不可或缺的作用。在这篇综述中，我们将 1) 讨论 TBI 后慢性炎症在神经精神症状发展中的当前证据，2) 强调潜在的小胶质细胞激活和细胞因子信号传导贡献，以及 3) 讨论免疫靶向干预和生物标志物策略的潜在前景和陷阱识别和治疗具有免疫相关神经精神症状的 TBI 患者。越来越多的证据表明，动物的免疫信号在严重压力或脑损伤后的抑郁和焦虑样行为中起着不可或缺的作用。在这篇综述中，我们将 1) 讨论 TBI 后慢性炎症在神经精神症状发展中的当前证据，2) 强调潜在的小胶质细胞激活和细胞因子信号传导贡献，以及 3) 讨论免疫靶向干预和生物标志物策略的潜在前景和陷阱识别和治疗具有免疫相关神经精神症状的 TBI 患者。越来越多的证据表明，动物的免疫信号在严重压力或脑损伤后的抑郁和焦虑样行为中起着不可或缺的作用。在这篇综述中，我们将 1) 讨论 TBI 后慢性炎症在神经精神症状发展中的当前证据，2) 强调潜在的小胶质细胞激活和细胞因子信号传导贡献，以及 3) 讨论免疫靶向干预和生物标志物策略的潜在前景和陷阱识别和治疗具有免疫相关神经精神症状的 TBI 患者。