Contribution of Inflammation to Chronic Pain Triggered by Nerve Injury

An injury to a peripheral nerve can be a slight stretch, a compression or a severe laceration. Such damage usually leads to an acute phase response characterized by nociceptive pain, inflammation and restriction of normal function. However, in about 7%-18% of the general population, pain persists, even after the injury healing, producing a state of chronic neuropathic pain. This type of hypersensitivity is debilitating and refractory to the majority of available analgesics. It adversely affects quality of life and bears a substantial cost to society. In the last two decades, compelling evidence strongly suggested that, in addition to changes in neuronal system, pathogenesis of neuropathic pain involves the interaction between the immune system and the nervous system. Inflammatory process alters local homeostasis and impairs neuronal function. In this chapter, we primarily focus on the evidence with experimental animal models obtained from our laboratory and from literature to highlight inflammatory reaction along the pain pathway (from damaged nerve to the spinal cord), and the critical role of this reaction in the development and maintenance of neuropathic pain. We also discuss the current progress and challenges of translating the inflammation related new targets into therapeutics.