Education  |   August 2018
Neuroinflammation and Central Sensitization in Chronic and Widespread Pain
Author Notes
  • From the Center for Translational Pain Medicine, Departments of Anesthesiology (R.-R.J., A.N., Y.H., N.T., W.M.); Neurobiology (R.-R.J.); and Pharmacology (A.N.), Duke University Medical Center, Durham, North Carolina.
  • This article is featured in “This Month in Anesthesiology,” page 1A.
    This article is featured in “This Month in Anesthesiology,” page 1A.×
  • Submitted for publication May 24, 2017. Accepted for publication January 12, 2018.
    Submitted for publication May 24, 2017. Accepted for publication January 12, 2018.×
  • Address correspondence to Dr. Ji: Duke University Medical Center, Durham, North Carolina 27710. Email: ru-rong.ji@duke.edu. Information on purchasing reprints may be found at www.anesthesiology.org or on the masthead page at the beginning of this issue. Anesthesiology’s articles are made freely accessible to all readers, for personal use only, 6 months from the cover date of the issue.
Article Information
Education / Review Article
Education   |   August 2018
Neuroinflammation and Central Sensitization in Chronic and Widespread Pain
Anesthesiology 8 2018, Vol.129, 343-366. doi:10.1097/ALN.0000000000002130
Anesthesiology 8 2018, Vol.129, 343-366. doi:10.1097/ALN.0000000000002130
Abstract

Chronic pain is maintained in part by central sensitization, a phenomenon of synaptic plasticity, and increased neuronal responsiveness in central pain pathways after painful insults. Accumulating evidence suggests that central sensitization is also driven by neuroinflammation in the peripheral and central nervous system. A characteristic feature of neuroinflammation is the activation of glial cells, such as microglia and astrocytes, in the spinal cord and brain, leading to the release of proinflammatory cytokines and chemokines. Recent studies suggest that central cytokines and chemokines are powerful neuromodulators and play a sufficient role in inducing hyperalgesia and allodynia after central nervous system administration. Sustained increase of cytokines and chemokines in the central nervous system also promotes chronic widespread pain that affects multiple body sites. Thus, neuroinflammation drives widespread chronic pain via central sensitization. We also discuss sex-dependent glial/immune signaling in chronic pain and new therapeutic approaches that control neuroinflammation for the resolution of chronic pain.