5-Year Study Unlocks Link Between Chronic Pain and Depression

For the first time, a direct biophysical link has been identified that connects chronic pain with mental health and substance abuse.

When chronic pain causes brain inflammation, it can lead to depression and anxiety, according to researchers from the University of California, Irvine (UCI) and Los Angeles (UCLA). Lead authors Catherine Cahill, PhD, Christopher Evans, PhD, along with colleagues discovered that pain activity can alter the mood and motivation regions in the brain — a finding that can help with the development of improved medication. In addition, the ineffective role of certain opioids in chronic pain relief was evaluated as well.

“For over 20 years, scientists have been trying to unlock the mechanisms at work that connect opioid use, pain relief, depression and addiction,” Cahill, associate professor of anesthesiology & perioperative care at UCI, said in a news release.

The brain inflammation caused by pain speeds up the growth and activation of microglia, immune cells that cause chemical signals in neurons to inhibit dopamine. Since this neurotransmitter is responsible for the reward and pleasure centers in the brain, the restriction can result in depression and anxiety.

“Our findings represent a paradigm shift which has broad implications that are not restricted to the problem of pain and may translate to other disorders,” Cahill said.

Despite the fact that pain medications like morphine are meant to stimulate the release of dopamine, the team discovered why it fails to stop discomfort. According to the report published in The Journal of Neuroscience, the drugs failed to do so in the mice models. However, the animals began experiencing reward-motivated behavior from the dopamine release once they were treated with a medication that stopped microglial activation.

Researchers are constantly developing strategies to relieve patients of chronic pain — such as using the shingles vaccine, caterpillar fungus, or spicy foods. These new findings provide a different approach to a condition that affects millions of people. Cahill and her team are now studying the association between changes in the brain caused by pain and mood disorders.

“We have a drug compound that has the potential to normalize reward-like behavior,” Cahill confirmed. “And subsequent clinical research could then employ imaging studies to identify how the same disruption in reward circuitry found in rodents occurs in chronic pain patients.”