Mar 21 (Reuters Health)--Physical pain is thought to originate in one area and travel to other parts of the body via nerve impulses. But according to scientists, pain may also be in the brain.
Their study in the March 22nd issue of Nature shows that common pain relievers known as nonsteroidal anti-inflammatory drugs (NSAIDs), such as aspirin and ibuprofen, may work better if researchers can find ways to get more of the drugs into the brain.
It was previously thought that pain traveled only through nerve impulses from the site of inflammation or injury, and many pain relievers are aimed at blocking nerve impulses at the site of inflammation.
The new study findings may help scientists develop more effective and safer drugs to treat pain, the report indicates.
"There clearly is a major central nervous system component in the way that the body responds to inflammation and this has a key role in the production of pain," Dr. Clifford Woolf, a study author from Massachusetts General Hospital in Boston, said in a prepared statement. "Now that we are starting to understand how local inflammation acts centrally, we need to...find ways to manage pain hypersensitivity more effectively."
To investigate the pathway from injury to pain, the researchers injected rats with a chemical that caused inflammation in the hind paws. The inflammation was found to cause an increase in levels of a molecule, interleukin-1B, in the fluid in the brain and spinal cord. This molecule causes fever, aches and pain throughout the body.
The rats' sensitivity to pain was inhibited when researchers injected a drug that blocked the molecule, suggesting that the higher levels of interleukin-1B in the brain and spinal cord are responsible for perceptions of pain.
Woolf's team also found that drugs aimed at cyclooxygenase-2 (Cox-2)--an enzyme blocked by aspirin and ibuprofen, as well as newer, more targeted pain relievers such as Vioxx and Celebrex--were more potent at lower doses when injected into the spinal cords of the rats. It seems that nerve impulses from the site of inflammation and injury may stimulate production of interleukin-1B, which in turn may increase production of Cox-2 throughout the central nervous system.
"These results suggest that inhibitors of cyclooxygenase-2 that better penetrate the blood-brain barrier would be even more efficient painkillers, working to block the oversensitivity to pain that is coordinated by the brain," Dr. Tamas Bartfai from The Scripps Research Institute in La Jolla, California, writes in an accompanying editorial.
The study was funded by National Institute of Neurological Disorders and Stroke.
SOURCE: Nature 2001;410:471-475,
2001 Reuters Ltd.