Preventing Brain Injury

If the scientists are correct that central pain involves an injury to the thalamus, either primarily as in stroke, or by referred exciter toxicity as in SCI, then blocking glutamate is of great importance in proventing brain injury.

Vivian Teichberg and associated scientists at the Weizman Weizmann Institute of Science in Israel have developed a method for ridding the brain of excess glutamate following a brain trauma. From all that is known, glutamate, the primary exciter of the central nervous system, is the mediator of exciter toxicity and changes which lead to central pain. (See eg. at this site, “We’ve learned that NMDA stinks…”)

The scientists at the Weizman Institute have found an enzyme in blood which will mop up excess amounts of glutamate in cases of brain injury. For those who presently have central pain, the damage is probably already done, but you never really know, until you try. For those injured in the future, this work from Israel may represent the best hope yet to avoid the spreading of injury in the brain which is the real enemy in any kind of brain trauma, including of course, the kind of injury which leads to central pain. Glutamate toxicity continues through the duration of central pain. Its release is linked to excess calcium, which in turn reaches NMDA and other pain exciter chemicals.

Glutamate spill activates NMDA which leads to spreading injury to the brain and also the potential for chronic central pain. Hence, it would be nice to eliminate toxic levels of glutamate which occur after brain or cord injury. It is not possible to eliminate glutamate from the brain, since ALL excitation revolves around the glutamate cycle. However, the Katrina-like flood of glutamate that occurs after brain injury injures surrounding tissue, expanding and amplifying the injury to the brain.

Most scientists feel the expanded injury represents the majority of damage in nearly all brain trauma. It also seems to blow out the pain circuits, which lose control, and then come back firing wildly under the influence of nerve repair and (neurotropic) growth factors. The process of repair is so disordered that it has the elements of inflammation. Indeed, some now feel central pain is a chronic neuroinflammatory state. Most chemicals of inflammation are also present in central pain. Soaking up excess glutamate may go a long way in either preventing or treating central pain.

It is heartening to see this type of work coming from countries around the world. However, there are a handful of brilliant scientists at NIH who should be funded for such studies. The “handful” is six scientists. It should be six thouaand. Indeed, for something as important as pain, and goodness knows the public is in semi-hysteria over opiates right now, it seems unexplainable that a serious project to end pain has not been funded at NIH/NIDCR. If opiates are so bad, let’s develop safer and nonaddictive ways to end pain.

Opiates are not typically effective for central pain, but so many of those suffering from post-SCI pain have ordinary mechanical pain that replacing opiates is relevant.

Being nice, patient, and passive has not produced results. It is to the public’s shame that those in agonizing central pain, and life debilitating mechanical pain are allowed to continue in that state with hardly a mention of solving it. The United States should show leadership, not a token effort. How long will philanthropic and charity groups ignore the plight of nerve injury pain? How long will the public look the other way? No one is saying “God wants the starving to be hungry”, so why do they say, “God wants those with severe nerve injury pain to be in agony”?