New drug-based approach could reduce chronic pain says study

An area of the brain that controls if we feel happy or sad, as well as addiction, seems to be remodeled by chronic pain, experts report in Nature Neuroscience.

And the team claims to have developed a new treatment strategy that restores this region and dramatically lessens pain symptoms in an animal model.

The treatment combines a Parkinson’s drug (L-dopa) and a non-steroidal anti-inflammatory drug. Together, the drugs target particular brain circuits in and completely eliminate chronic pain behaviour when given to rodents with chronic pain. So far, the key has been administering the drugs together and shortly after an injury.

Scientists are now looking to test the approach on people as they think the treatment has the potential to prevent chronic pain if used early enough after injury.

“It was surprising to us that chronic pain actually rewires the part of the brain controlling whether you feel happy or sad,” explains Dr D James Surmeier, who is involved in the work.

“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.”

Another author, Prof A Vania Apkarian, comments:

“The study shows you can think of chronic pain as the brain getting addicted to pain. The brain circuit that has to do with addiction has gotten involved in the pain process itself.”

The experts found that a group of brain cells believed to be responsible for negative emotions became hyper-excitable and more strongly connected with other regions of the brain linked to feeling bad within days after an injury that triggers chronic pain behavior.

This change seems to be triggered by a drop in dopamine, which transmits messages between brain cells.

When scientists administered the non-steroidal anti-inflammatory drug and L-dopa, which raises dopamine levels, the changes in the brain were reversed and the animals’ chronic pain behaviour stopped.

“These results establish chronic pain cannot be viewed as a purely sensory phenomenon but instead is closely related to emotions,” Prof Apkarian says.

Scientists also treated rats in chronic pain with another Parkinson’s drug (pramipexole) that activated dopamine receptors, copying dopamine’s effect. This drug also decreased the animals’ pain-like behaviour.

So supplementing anti-inflammatories with a medication that activates dopamine receptors or raises dopamine levels might become an effective way of treating chronic pain and/or preventing a transition to chronic pain after injury.

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