A new study published in Reuters Health suggests that doctors may soon have another area to target when it comes to treating chronic pain: your brain’s glial cells.
Researchers said their study indicated that patients with chronic pain often show signs of glial cell activation in areas of the brain that modulate pain.
“Glia appears to be involved in the pathophysiology of chronic pain, and therefore we should consider developing therapeutic approaches targeting glia,” said Dr. Marco L. Loggia, of Massachusetts General Hospital. “Glial activation is accompanied by many cellular responses, which include the production and release of substances (such as so-called ‘pro-inflammatory cytokines’) that can sensitize the pain pathways in the central nervous system. Thus, glial activation is not a mere reaction to a pain state but actively contributes to the establishment and/or maintenance of persistent pain.”
To test the theory that chronic pain sufferers experience activation of brain glia, Dr. Loggia and his team analyzed data from 19 patients with chronic low back pain and 25 non-chronic pain volunteers. After analyzing translocator protein (TPSO) levels associated with the activation of brain glia, researchers found:
- Protein increases were significantly higher in patients with chronic low back pain than in the control group.
- There were no brain regions in which the control group experienced a higher protein presence than the chronic back pain group.
“It’s important to stress that although TSPO upregulation is a marker of glial activation and therefore of a pro-inflammatory state, animal studies suggest that its role is actually to limit the magnitude of glial responses after their initiation, thereby promoting the return to pre-injury pain-free status and recovery from pain,” said Dr. Loggia. “This means that what we are imaging may be the process of glial cells trying to ‘calm down’ after being activated by the pain. Thus, subjects with low levels of pain-related TSPO upregulation on activated glia may be less able to adequately inhibit neuroinflammatory responses, and have a more exaggerated response that ultimately leads to more inflammation and pain.”
Dr. Loggia continued:
“No objective biomarkers exist to determine if somebody is in pain (i.e. you can’t just hook someone up to a machine to see if they’re experiencing chronic pain). Thus, this study – aside from suggesting glia as a therapeutic target for pain – is important as it may provide an important step toward the identification of objective biomarkers for pain conditions.”
He concluded by saying knowledge of human glial activation had been limited, prior to the study.
“In animal studies we know that glial modulators, which limit glial activation, can potently inhibit or reverse pain,” Dr. Loggia said. “However, evidence of glial involvement in human pain has been very limited until now. Observing glial activation in humans has important potential implications for the development of new therapies based on glial modulation. Seeing that glial activation really happens in patients will provide the rationale to justify a more aggressive exploration of this therapeutic route, and identify which patients are more likely to benefit from these types of therapies.”
Related source: Reuters, Scientific American
Thomas Cohn, MD
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