Department of Neuroscience, Central Clinical School/Monash University, Melbourne, Victoria, Australia.
Department of Psychology, Alberta Children's Hospital Research Institute, Hotchkiss Brain Institute/The University of Calgary, Calgary, Alberta, Canada.
Dev Neurosci. 2020;42(1):2-11. doi: 10.1159/000508663. Epub 2020 Jul 10.
Pain is evolutionarily necessary for survival in that it reduces tissue damage by signaling the body to respond to a harmful stimulus. However, in many circumstances, acute pain becomes chronic, and this is often dysfunctional. Adolescent chronic pain is a growing epidemic with an unknown etiology and limited effective treatment options. Given that the relationship between acute pain and chronic pain is not straightforward, there is a need to better understand the factors that contribute to the chronification of pain. Since early life factors are critical to a variety of outcomes in the developmental and adolescent periods, they pose promise as potential mechanisms that may underlie the transition from acute to chronic pain. This review examines two early life factors: poor diet and adverse childhood experiences (ACEs); they may increase susceptibility to the development of chronic pain following surgical procedures or traumatic brain injury (TBI). Beyond their high prevalence, surgical procedures and TBI are ideal models to prospectively understand mechanisms underlying the transition from acute to chronic pain. Common themes that emerged from the examination of poor diet and ACEs as mechanisms underlying this transition included: prolonged inflammation and microglia activation leading to sensitization of the pain system, and stress-induced alterations to hypothalamic-pituitary-adrenal axis function, where cortisol is likely playing a role in the development of chronic pain. These areas provide promising targets for interventions, the development of diagnostic biomarkers, and suggest that biological treatment strategies should focus on regulating the neuroinflammatory and stress responses in an effort to modulate and prevent the development of chronic pain.
疼痛在进化上是生存所必需的，因为它通过向身体发出信号来对有害刺激做出反应，从而减少组织损伤。然而，在许多情况下，急性疼痛会变成慢性疼痛，而且这种疼痛往往是功能失调的。青少年慢性疼痛是一种日益严重的流行疾病，其病因不明，有效治疗方法有限。鉴于急性疼痛和慢性疼痛之间的关系并不简单，因此需要更好地了解导致疼痛慢性化的因素。由于生命早期的因素对发育和青少年时期的各种结果至关重要，因此它们有可能成为从急性疼痛向慢性疼痛转变的潜在机制。这篇综述探讨了两个生命早期的因素：不良饮食和不良童年经历 (ACEs)；它们可能会增加在接受手术或创伤性脑损伤 (TBI) 后发生慢性疼痛的易感性。除了它们的高患病率之外，手术和 TBI 是前瞻性了解从急性到慢性疼痛转变的潜在机制的理想模型。从不良饮食和 ACEs 作为这种转变的潜在机制的检查中出现的共同主题包括：炎症和小胶质细胞激活的持续时间延长导致疼痛系统的致敏，以及应激诱导的下丘脑-垂体-肾上腺轴功能改变，其中皮质醇可能在慢性疼痛的发展中起作用。这些领域为干预措施、诊断生物标志物的开发提供了有希望的目标，并表明生物治疗策略应侧重于调节神经炎症和应激反应，以努力调节和预防慢性疼痛的发展。
