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Neuroinflammation and Chronic Pain

By: , Posted on: January 30, 2015

Brain_ScanIn a recent study from Massachusetts General Hospital (MGH), an affiliate of Harvard, scientists have found evidence of neuroinflammation in key regions of the brains of patients with chronic pain. The study, published in BRAIN, shows that levels of an inflammation-linked protein are elevated in regions known to be involved in the transmission of pain, the study paves the way for the exploration of potential new treatment strategies and identifies a possible way around one of the most frustrating limitations in the study and treatment of chronic pain, the lack of an objective way to measure the presence or intensity of pain.

Carl Saab, Assistant Professor of Neurosurgery (Research), Assistant Professor of Neuroscience, Brown University, comments on this study:

The main significance of this study is the non-invasive visualization of a microglial response in the brains of pain patients. Findings from this study corroborate those from my lab using an animal model (Neurosci Lett. 2011 Jul 8;498(2):138-42. doi: 10.1016/j.neulet.2011.04.077. Epub 2011 May 6. Minocycline injection in the ventral posterolateral thalamus reverses microglial reactivity and thermal hyperalgesia secondary to sciatic neuropathy. LeBlanc BW, Zerah ML, Kadasi LM, Chai N, Saab CY.).

This opens the door to potentially exciting therapeutic and diagnostic advances in an otherwise stagnant field. It also points to a paradigm shift in focusing on brain abnormalities in relation to chronic pain, the topic of my recent book, Chronic Pain and Brain Abnormalities.

A few cautionary points are worth mentioning:

  • The evidence is secondary, i.e based on a transporter protein linked to microglia
  • Qualifying microglia as ‘activated’ is contentious since this term requires multi-step verification of cell morphology and physiology
  • Microglial ‘hyperactivity’ does not necessarily equate with ‘neuro-inflammation’
  • This is an observation that does not allow us to draw conclusions about functional significance (does this phenomenon contribute to or oppose pain?).

Lastly, contrary to some recent commentaries, this is not the only study that claims to have imaged glia in humans in vivo (see reference related to a PET-imaged radio-ligand ([11C]-(R)-PK11195) linked to activated microglia (Br Med Bull.2003;65:121-31. Neuropathological imaging: in vivo detection of glial activation as a measure of disease and adaptive change in the brain. Banati RB).

About the Book:

chronic pain and brain abnormalitiesIt is only natural for someone in pain to attend to the body part that hurts. Yet this book tells the story of persistent pain having negative effects on brain function. The contributors, all leading experts in their respective fields of pain electrophysiology, brain imaging, and animal models of pain, strive to synthesize compelling and, in some ways, connected hypotheses with regard to pain-related changes in the brain.

Together, they contribute their clinical, academic, and theoretical expertise in a comprehensive overview that attempts to define the broader philosophical context of pain (disentangling sensical from nonsensical claims), list the changes known to take place in the brains of individuals with chronic pain and animal models of pain, address the possible causes and mechanisms underlying these changes, and detail the techniques and analytical methods at our disposal to “visualize” and study these changes.

To purchase your copy of Chronic Pain and Brain Abnormalities visit the Elsevier Store. Apply discount code NEURO215 to save 25% off list price and free global shipping.

About the Author:

3483-Editor-PhotoCarl Saab is a PhD Neuroscientist studying neurological disorders in model systems. He obtained his PhD in 2001 from the University of Texas Medical Branch in pain research mapping pain pathways in the CNS (thesis advisor WD Willis). He then completed his postdoctoral fellowship in the laboratory of Stephen Waxman at Yale studying sodium channelopathies in pain and multiple sclerosis. Currently Carl is Assistant Professor at Brown University & Rhode Island Hospital, Neurosurgery and Neuroscience.

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