There is a high co-occurrence of risky substance use among adults with traumatic brain injury (TBI), although it is unknown if the neurologic sequelae of TBI can promote this behavior. We propose that to conclude that TBI can cause risky substance use, it must be determined that TBI precedes risky substance use, that confounders with the potential to increase the likelihood of both TBI and risky substance use must be ruled out, and that there must be a plausible mechanism of action. In this review, we address these factors by providing an overview of key clinical and preclinical studies and list plausible mechanisms by which TBI could increase risky substance use. Human and animal studies have identified an association between TBI and risky substance use, although the strength of this association varies. Factors that may limit detection of this relationship include differential variability due to substance, sex, age of injury, and confounders that may influence the likelihood of both TBI and risky substance use. We propose possible mechanisms by which TBI could increase substance use that include damage-associated neuroplasticity, chronic changes in neuroimmune signaling, and TBI-associated alterations in brain networks.

在患有创伤性脑损伤 (TBI) 的成年人中，使用危险物质的几率很高，尽管尚不清楚 TBI 的神经系统后遗症是否会促进这种行为。我们建议得出 TBI 会导致危险物质使用的结论，必须确定 TBI 先于危险物质使用，必须排除可能增加 TBI 和危险物质使用可能性的混杂因素，并且必须有一个合理的作用机制。在这篇综述中，我们通过提供关键临床和临床前研究的概述来解决这些因素，并列出 TBI 可能增加危险物质使用的似是而非的机制。人类和动物研究已经确定了 TBI 与危险物质使用之间的关联，尽管这种关联的强度各不相同。可能限制这种关系检测的因素包括由于物质、性别、受伤年龄和可能影响 TBI 和危险物质使用可能性的混杂因素引起的差异变异性。我们提出了 TBI 可以增加物质使用的可能机制，包括与损伤相关的神经可塑性、神经免疫信号的慢性变化以及脑网络中与 TBI 相关的改变。