NSAIDs reduce sensitivity of nerves in the central nervous system by inhibiting production of the Cox-2 enzyme responsible for pain and inflammation. Two prescription drugs introduced last year that target Cox-2 proved to be blockbuster pain relievers, but their mechanism of action was not understood until now.
A research team led by Clifford J. Woolf, M.D., Ph.D., at Massachusetts General Hospital in Boston used an animal model to study Cox-2's role in inflammatory pain. When inflammation occurred, researchers found Cox-2 throughout the central nervous system, as well as at the local site of inflammation. They also found that inhibiting Cox-2 production within the spinal cord and brain decreased pain and reduced hypersensitivity to normal sensations such as touch. Researchers now believe the widespread distribution of Cox-2 within the central nervous system may contribute to muscle and joint pain, depression, lethargy, and loss of appetite that often occur with inflammation and infection.
"The findings indicate new treatment options for arthritis and other inflammatory pain conditions," said Cheryl A. Kitt, Ph.D., program director for pain research at the NINDS. "Targeting the central nervous system when using NSAIDs, rather than the specific peripheral pain site, may result in more effective pain relief."
The NINDS, part of the National Institutes of Health in Bethesda, Maryland, is the nation's leading supporter of research on the brain and nervous system. The NINDS is now celebrating its 50th anniversary.
This release will be posted on EurekAlert! at http://www.eurekalert.org and on the NINDS website at http://ninds.nih.gov/news_and_events/index.htm.