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Discovery May Help Doctors Curb Pain : Medicine: Researchers find that aspirin aids in blocking increased sensitivity after injury or surgery.

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TIMES STAFF WRITER

Scientists have discovered that aspirin acts on the spinal cord to help block the increased sensitivity to pain that people experience after surgery or an injury--a finding that may offer doctors a new avenue in curbing pain, a San Diego researcher reported Friday.

While doctors have believed that aspirin and other non-steroidal drugs ease pain by reducing the inflammation at the injured area, they now believe aspirin also affects the central nervous system by preventing the release of a chemical messenger that increases sensitivity to pain.

“This gives us another tool to control pain, a tool that is not a narcotic,” said Dr. Harvey Shapiro, chairman and professor at UC San Diego’s department of anesthesiology. “I look at it as a palette and I’ve got another color to use. That is exciting.”

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Scientists have long tried to crack the secret to pain. Why, for instance, do people feel more susceptible to pain after they break a leg?

Pain has different stages. When you break a bone, you feel sharp, intense pain. Unchecked, that pain will evolve into a low-level throbbing, which is also what you feel after surgery. At this stage, known as hyperalgesia, your sensitivity to pain is dramatically heightened. In the wrestling ring with pain, this would be Round 2.

Tony Yaksh, a UCSD professor of anesthesiology, is trying to understand the mechanism that controls hyperalgesia. He and others now believe that pain occurs when certain substances, such as prostaglandins, gather at the site of an injury. Prostaglandins act as chemical messengers to the spinal cord, and their signal is simple: OW!

Researchers are finding that such activity causes the spinal cord to release neurotransmitters, which, in turn, means that any stimulation to the injured area causes a dramatic increase in the pain an injured person experiences.

In a study released Friday in the journal Science, Yaksh and co-author Annika Malmberg finger prostaglandins as the culprit most likely to cause increased sensitivity at the site of an injury.

“Early studies with aspirin showed that it blocks the formation of prostaglandins and that prostaglandins gather at the site of injury and cause inflammation. This led to the belief that aspirin and other non-steroidal anti-inflammatory drugs reduce pain by direct action at the site of injuries which involve inflammation,” said Malmberg, a visiting doctoral candidate from Gothenberg, Sweden.

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“In contrast, our study shows that aspirin also inhibits pain processing at the spinal cord level, and it is in fact at this site where it can help decrease hyperalgesia,” Malmberg said.

If scientists could nip this pain cycle before it reaches hyperalgesia, they might dramatically reduce the agony of, say, a broken leg.

“It’s a rewiring that obviously contributes to more suffering and more pain. If you treat this early, if you prevent it from getting started, the overall pain can be considerably decreased,” said Shapiro, who also runs UCSD’s pain medicine group. “We would be preventing the cycle of pain from starting.”

The discovery may also lead doctors to rethink their strategy of curbing pain after surgeries.

“We are beginning to find that pain messages at the time of injury initiate hyperalgesia,” Yaksh said. “For people undergoing surgery, it may be best to block this process before surgery. This serves to eliminate some of the pain people experience when recovering from surgery.

“Obviously, for people who experience unexpected injury, we have to find some way to inhibit hyperalgesia after it has been initiated. If we can identify other mediators such as prostaglandins that are necessary to sustain hyperalgesia, we may be able to develop better medications . . . and reduce increased sensitivity to pain following injury.”

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