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.
Dev Neurosci

中文翻译：

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创伤性脑损伤和手术后青少年慢性疼痛的发展：饮食和早期生活压力的作用。

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对有害刺激做出反应来减少组织损伤。然而，在许多情况下，急性疼痛会变成慢性疼痛，这通常是功能失调的。青少年慢性疼痛是一种日益流行的流行病，病因不明，有效的治疗选择有限。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。由于早期生活因素对发育和青少年时期的各种结果至关重要，因此它们有望成为潜在的机制，可能是从急性疼痛过渡到慢性疼痛的基础。本综述考察了两个早期生活因素：不良饮食和不良童年经历 (ACE)；它们可能会增加在外科手术或创伤性脑损伤 (TBI) 后发生慢性疼痛的易感性。除了高患病率之外，外科手术和 TBI 是理想的模型前瞻性地了解从急性疼痛到慢性疼痛转变的潜在机制。从检查不良饮食和 ACE 作为这一转变机制的常见主题包括：长期的炎症和小胶质细胞激活导致疼痛系统敏感，以及压力引起的下丘脑 - 垂体 - 肾上腺轴功能的改变，其中皮质醇可能在慢性疼痛的发展中发挥作用。这些领域为干预、诊断生物标志物的开发提供了有希望的目标，并建议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。
开发神经科学