Boulder – Morphine works wonders for a broken bone, but barely takes the edge off the phantom pain of an amputated limb.
Chronic pain is notoriously difficult to treat, and University of Colorado psychologist Linda Watkins thinks she knows why. Her answer has the potential to change the way doctors manage patient pain.
“It’s the glia,” Watkins said, referring to a class of cells that has suddenly emerged as the hottest target of anti-pain medicine.
“Glia don’t like morphine. It irritates them,” Watkins said.
Irritated glial cells, Watkins has discovered, mess with the ability of morphine to calm down everyday pain neurons.
A research team, including Watkins, reports its findings in a paper scheduled for the December issue of the academic journal Trends in Neuroscience.
The research could help explain why opiate withdrawal is so painful.
It has already spawned a business connection between Watkins and the California company Avigen Inc., which is studying two drugs to calm down overexcited glia.
Drugs currently used to manage chronic pain are woefully inadequate, Watkins said. For the ongoing agony of a back injury, an amputation or chemotherapy, pain drugs considered “good” still fail 60 percent to 80 percent of the time, she said. Chronic-pain victims respond poorly to opiates, or need very high doses, she said.
“It’s a horrible situation. These are not minor issues. These are people who commit suicide,” Watkins said.
The American Pain Foundation estimates that one in four U.S. adults suffers chronic pain, and for some, it’s completely debilitating.
Robert Schwartzman, chair of the neurology department at the Drexel University College of Medicine in Philadelphia, works with people who develop a complicated pain syndrome after seemingly minor injuries, such as whiplash.
“They get narcotics but they remain in terrible pain,” Schwartzman said. “They sit home and lose their jobs and friends.”
Schwartzman and others have known for several years that certain chemicals – called cytokines – are somehow involved in that ongoing pain, but it took Watkins to explain how.
Glial cells, which become overactive during exaggerated pain responses, pump out cytokines, she found. Opiate drugs make it worse, exciting glia and counteracting the effect of the pain drug.
“That’s a really major advance,” Schwartzman said. “Now we’re finally starting to understand this pain business.”
Watkins used a gene-therapy technique to treat overexcited glial cells in laboratory rats suffering chronic pain, with clear results. She injected genes that coax spinal cells to make anti-inflammatory cytokines. The treatment calmed the glial cells, but didn’t affect normal pain neurons.
Rats that previously avoided using a painful paw began running around, Watkins said. “We turned off neuropathic pain completely.”
Watkins said she expects Avigen to begin clinical trials with a similar technique next year.
Staff writer Katy Human can be reached at 303-820-1910 or khuman@denverpost.com.
