One of the big challenges of medicine has been to figure out what causes pain to become chronic. How can two people have the same exact injury and yet one person have a full recovery while the other’s pain continues to linger and becomes unrelenting? Why does one sprained ankle get better after a few weeks while another turns into a debilitating chronic pain syndrome?
While for centuries doctors have understood the basic process of acute pain that occurs after tissue damage — swelling, heat, redness, sensitivity– solving the mystery of why in some cases the pain does not resolve has remained elusive. But surely unlocking this mystery holds the promise of potentially preventing a disease more common than diabetes, cancer, strokes, and heart disease combined– chronic pain!
Fortunately, a greater understanding of what causes acute pain to evolve into chronic pain seems to be now taking place. And a big part of what causes the pain to persist seems to come from an unlikely source, namely, glial cells. Glial cells have historically been thought of as support structures for neurons inside the brain, but the real action of what happens was always thought to revolve around what the neurons do, as they contain the neurotransmitters that conduct information while glial cells do not.
But now it appears that when it comes to chronic pain that glial cells do much more than provide housekeeping support to nerves. In fact research done over the last decade suggest that glial cells are what cause neurons to become over-active inside the brain and spinal cord, making them super-sensitive to pain and perpetuating the pain message. The glial cells cause this disruption in normal nerve function by releasing inflammatory mediators that enhance pain.
Linda Watkins at the University of Colorado has been one of the leaders in researching how glial cells affect pain. Laboratory studies seem to show that blocking the release of pro-inflammatory mediators from glial cells can inhibit a variety of pain states. Once an injury takes place, the inflamed tissue activates the body’s immune system which in turn triggers the glia cells to switch to “pain mode” and that leads to over-excitation of pain pathway nerves in the central nervous system. Once turned on, the glia cells keep the nerves in pain mode.
Now the story gets even more sinister. Not only do glial cells seem to play an important role in perpetuating pain, but they also seem to play an integral part in developing tolerance to opiate pain medications, thereby blocking their effectiveness. Opiates, like morphine, bind to receptors on glial cells, but instead of causing them to quiet down, the morphine actually activates the glial cells to go into “pain mode” so that they release more and more pro-inflammatory mediators which make the pain get worse, as opposed to relieved.
These glial cell discoveries have prompted some researchers to shift their focus from treating the neurons themselves to finding ways to better regulate the glial cells with the hope of preventing or turning off pain states.
Peter Abaci, MD, is certified in anesthesia and pain management by the American Board of Anesthesiology. He serves as the Medical Director of the nationally recognized Bay Area Pain and Wellness Center, located in Los Gatos, California.
Dr. Abaci focuses on developing alternative solutions to treating chronic pain by drawing on neuroscience research, evidence-based medicine, ancient healing remedies, stress management techniques, nutrition principles, exercise programs, art therapy, and real-life lessons.
This column is republished with the permission of Pain Relief Revolution.