A brain region controlling whether we feel happy or sad, as well as addiction, is remodeled by chronic pain, reports a new Northwestern Medicine study.
And in a significant breakthrough for the millions of Americans suffering from chronic pain, scientists have developed a new treatment strategy that restores this region and dramatically lessens pain symptoms in an animal model.
The new treatment combines two FDA-approved drugs: a Parkinson’s drug, L-dopa, and a nonsteroidal anti-inflammatory drug. The combined drugs target brain circuits in the nucleus accumbens and completely eliminate chronic pain behavior when administered to rodents. The key is administering the drugs together and shortly after an injury.
As a result of the study’s findings, the scientists are pursuing a clinical trial. The treatment has the potential to prevent chronic pain if used early enough after injury, the scientists said.
The study was published December 21 in Nature Neuroscience.
“It was surprising to us that chronic pain actually rewires the part of the brain controlling whether you feel happy or sad,” said corresponding author D. James Surmeier, PhD, chair of physiology at Northwestern University Feinberg School of Medicine (Feinberg). “By understanding what was causing these changes, we were able to design a corrective therapy that worked remarkably well in the models. The question now is whether it will work in humans.”
“The study shows you can think of chronic pain as the brain getting addicted to pain,” said A. Vania Apkarian, PhD, also a corresponding author and a professor of physiology at Feinberg. “The brain circuit that has to do with addiction has gotten involved in the pain process itself.”
A group of neurons thought to be responsible for negative emotions became hyperexcitable and more strongly connected with other regions of the brain linked to feeling bad within days after an injury that triggered chronic pain behavior, the study showed. It went on to show that this change was triggered by a drop in dopamine, a critical neurotransmitter.
When scientists administered the nonsteroidal anti-inflammatory drug and L-dopa, which raises dopamine levels, the changes in the brain were reversed and the animals’ chronic pain behavior stopped.
“These results establish chronic pain cannot be viewed as a purely sensory phenomenon but instead is closely related to emotions,” Apkarian said.
In addition, the scientists treated rats experiencing chronic pain with another Parkinson’s drug, pramipexole, that activated dopamine receptors, mimicking dopamine’s effect. This drug also decreased the animals’ painlike behavior.
Currently, the most common treatment for chronic pain is a nonsteroidal anti-inflammatory type of drug, which has limited effectiveness.
The results of the study suggest that supplementing anti-inflammatories with a medication that activates dopamine receptors or raises dopamine levels might be more effective in treating chronic pain and/or preventing a transition to chronic pain.
This article was adapted from information provided by Northwestern University.