Scientists Unlock The Mystery Of Nerve Pain
posted 08/25/03
Experts believe they are a step closer to solving the riddle of the severe "neuropathic" pain.

The pain is caused by subtle nerve damage, can often be agonizing, and frequently does not improve over time. However, scientists at the National Institute of Health Sciences in Tokyo may have helped reveal a little about the physical mechanism behind the pain. Their findings could eventually lead to new drugs to ease the condition. A variety of physical conditions appear to be able to trigger the nerve damage, which causes pain.

Viral infections such as shingles, surgery and diabetes have all been known to lead to the problem. In some cases, even the slightest touch can produce excruciating pain.

Scientists are still struggling to exactly why such a powerful pain message is sent back to the brain. But, the answer may lie in "microglial" cells - which can be found in the spinal cord and behave a little like immune cells. They appear to congregate at sites where there is damage, perhaps playing some role in the repair process. When the Tokyo researchers took activated microglial cells, then injected them directly into the spinal cords of rats, they developed neuropathic pain.

The researchers believe that a particular receptor protein on the surface of the cell may be responsible. When rats were given nerve damage so that they developed neuropathic pain without the injections, high concentrations of this protein were found.

There is now the possibility - that if the same protein exists in humans - that a drug could be developed to block its effect. This might reduce the level of pain suffered.

We could be looking at a mechanism which will help us understand what is happening in neuropathic pain. "Very often the only drugs that we find will offer any relief to patients are antidepressants, and we don't know why this should work - but this could help explain it," stated Dr Donna Lloyd, from the Pain Research Institute at Liverpool University.

Source: Diabetes In Control Dot Com.

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