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Glial Cells: A New Target for Chronic Pain Treatment
cweinbl posted:
Glial cells are promising targets for the treatment of chronic neuropathic pain, according to Linda R. Watkins, PhD. Suppressing glial cell activation, she believes, may pave the way for the development of new drugs, increase the efficacy of opioids, and reduce drug dependence and tolerance.Research during the past two decades has shown that glial cells are important players in the creation and maintenance of pathologic pain states, and now perhaps in headache and trigeminal neuropathy as well. More recent work has demonstrated that glial cells dysregulate the actions of opioids such as morphine, a finding that has dramatic implications for the treatment of pain.

"The data clearly predict that targeting glial cells and their proinflammatory products will provide superior pain control," said Dr. Watkins, at the Headache Cooperative of the Pacific's 2009 Winter Colloquium. Glial cell activation has been demonstrated in every clinically relevant animal model study to date, including that of peripheral nerve injury, bone cancer, multiple sclerosis (MS), spinal cord injury, herniated disks, low back pain, and migraine, noted Dr. Watkins, Professor of Psychology and Neuroscience at the University of Colorado at Boulder. "Targeting the glial cells and their proinflammatory products doesn't make a patient analgesic, and it doesn't suppress all pain sensitivity. It simply returns the pain to normal. It removes the abnormal pain, which is a good thing. We don't want the patients walking around oblivious to all pain?. If you block these proinflammatory cytokines, you return the pain patient to being normal."

Read the entire article in Neurology Reviews here: .
bren_bren responded:
I really enjoyed this article, thanks for sharing Charles, B
cweinbl replied to bren_bren's response:
My pleasure. I devote a lot of time to pain research. Whenever I discover something pertinent, I like to share it with this intelligent group. I hope that others will do the same.

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