Abstract
Pain, especially chronic pain, is one of the most common clinical symptoms and has been considered as a worldwide healthcare problem. The transition from acute to chronic pain is accompanied by a chain of alterations in physiology, pathology, and psychology. Increasing clinical studies and complementary animal models have elucidated effects of stress regulation on the pain chronification via investigating activations of the hypothalamic-pituitary-adrenal (HPA) axis and changes in some crucial brain regions, including the amygdala, prefrontal cortex, and hippocampus. Although individuals suffer from acute pain benefit from such physiological alterations, chronic pain is commonly associated with maladaptive responses, like the HPA dysfunction and abnormal brain plasticity. However, the causal relationship among pain chronification, stress regulation, and brain alterations is rarely discussed. To call for more attention on this issue, we review recent findings obtained from clinical populations and animal models, propose an integrated stress model of pain chronification based on the existing models in perspectives of environmental influences and genetic predispositions, and discuss the significance of investigating the role of stress regulation on brain alteration in pain chronification for various clinical applications.
Highlights
Chronic pain is a main source of worldwide disability, causing physical and psychological discomforts and rising huge medical expenses [1]
Melzack [2] proposed that stress played an important role in such pain chronification, and accumulating evidence demonstrated that stress regulation consistently engaged in the development of chronic pain [3,4,5]
We have provided a broad range of compelling evidence that pain modulation and stress regulation can be considered as an integrated processing [2], within the framework of corticolimbic system
Summary
Chronic pain is a main source of worldwide disability, causing physical and psychological discomforts and rising huge medical expenses [1]. Melzack [2] proposed that stress played an important role in such pain chronification, and accumulating evidence demonstrated that stress regulation (as indexed by the function of hypothalamic-pituitary-adrenal [HPA] axis) consistently engaged in the development of chronic pain [3,4,5] In line with these findings, several brain regions, subserving as key candidates for stress regulation [6,7,8], have been reported to be involved in the transition from acute to chronic pain, including the amygdala, prefrontal cortex (PFC), and hippocampus [9,10,11,12]. We discuss two existing stress models of chronic pain in perspectives of environmental influences and genetic predispositions, respectively, and propose an integrated stress model of pain chronification based on previous findings
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