Announcement

Collapse
No announcement yet.

The Role of Stress Regulation on Neural Plasticity in Pain Chronification

Collapse
X
  • Filter
  • Time
  • Show
Clear All
new posts

  • Ref The Role of Stress Regulation on Neural Plasticity in Pain Chronification

    The Role of Stress Regulation on Neural Plasticity in Pain Chronification

    Xiaoyun Li and Li Hu, Neural Plast. 2016

    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.

    Introduction

    Chronic pain is a main source of worldwide disability, causing physical and psychological discomforts and rising huge medical expenses [1]. Understanding mechanisms of the development of chronic pain is crucial in monitoring and preventing the progress of pain chronification. In recent decades, increasing clinical studies and complementary animal models contributed to important advances in understanding the transition from acute to chronic pain. Notably, 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 [3–5]. In line with these findings, several brain regions, subserving as key candidates for stress regulation [6–8], have been reported to be involved in the transition from acute to chronic pain, including the amygdala, prefrontal cortex (PFC), and hippocampus [9–12]. Therefore, some previous studies hypothesized that these brain regions, especially within the emotional corticolimbic system, acted as the bridge of pain modulation and stress regulation. In this paper, we briefly walk through concepts of pain and stress, review effects of the HPA function on acute and chronic pain, and discuss alterations of stress-associated brain regions in acute and chronic pain. In the following, 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.
    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5178373/
    Marcel

    "Evolution is a tinkerer not an engineer" F.Jacob
    "Without imperfection neither you nor I would exist" Stephen Hawking
Previously entered content was automatically saved. Restore or Discard.
Auto-Saved
x
Insert: Thumbnail Small Medium Large Fullsize Remove  
x
x
Working...
X