Neuroinflammation and Central Sensitization in Chronic and Widespread Pain
PainSci summary of Ji 2018?This page is one of thousands in the PainScience.com bibliography. It is not a general article: it is focused on a single scientific paper, and it may provide only just enough context for the summary to make sense. Links to other papers and more general information are provided at the bottom of the page, as often as possible.
original abstract†Abstracts here may not perfectly match originals, for a variety of technical and practical reasons. Some abstacts are truncated for my purposes here, if they are particularly long-winded and unhelpful. I occasionally add clarifying notes. And I make some minor corrections.
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.
related content
- “An evolutionary stress-response hypothesis for chronic widespread pain (fibromyalgia syndrome),” Pamela Lyon, Milton Cohen, and John Quintner, Pain Med, 2011.
- “Brain glial activation in fibromyalgia - A multi-site positron emission tomography investigation,” Daniel S Albrecht, Anton Forsberg, Angelica Sandström, Courtney Bergan, Diana Kadetoff, Ekaterina Protsenko, Jon Lampa, Yvonne C Lee, Caroline Olgart Höglund, Ciprian Catana, Simon Cervenka, Oluwaseun Akeju, Mats Lekander, George Cohen, Christer Halldin, Norman Taylor, Minhae Kim, Jacob M Hooker, Robert R Edwards, Vitaly Napadow, Eva Kosek, and Marco L Loggia, Brain Behav Immun, 2019.
- “Evolution, Stress and Fibromyalgia,” John Quintner, FMperplex.com.
Specifically regarding Ji 2018:
- “Fibromyalgia and Neuroinflammation: Shall the Twain Ever Meet?,” John Quintner, FMperplex.com.
These two articles on PainScience.com cite Ji 2018 as a source:
- PS 33 Surprising Causes of Pain — Trying to understand pain when there is no obvious explanation
- PS Chronic, Subtle, Systemic Inflammation — One possible sneaky cause of puzzling chronic pain
This page is part of the PainScience BIBLIOGRAPHY, which contains plain language summaries of thousands of scientific papers & others sources. It’s like a highly specialized blog. A few highlights:
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- Agreement of self-reported items and clinically assessed nerve root involvement (or sciatica) in a primary care setting. Konstantinou 2012 Eur Spine J.
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- Association of Spinal Manipulative Therapy With Clinical Benefit and Harm for Acute Low Back Pain: Systematic Review and Meta-analysis. Paige 2017 JAMA.