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In short, he has become the most recognized person in a wheelchair ever--even more familiar than Franklin Roosevelt, who concealed his chair from public view. Reeve did not want to become the poster boy for America's quadriplegics. He wanted to be a symbol of potential recovery. "People like me sometimes complain, 'When you say I'm in a wheelchair, you imply that there's something wrong with me.' Well, there is. My response is that we're entitled to something more in life."
He says, "Juice would always tell me, 'You've been to the grave two times this year, brother. You're not going there again. You are here for a reason.' And my answer was, no, I wasn't injured for a reason. It was an accident, it just happened. But now I have the opportunity to make sense out of it. I believe it's what you do after a disaster that gives it meaning."
However quiet and hidden it may have been, a good deal of progress has been made in the treatment of spinal-cord injuries, and Reeve's injury is coincidental with the period of greatest progress in the research. A few years ago, researchers knew only that it was necessary to preserve as many nerves as possible in the early stages of an injury. They believed that whatever nerves were lost were lost permanently. Now, says Young, they are talking about working with a much greater number of cells because they are convinced that axons can and will grow. This understanding has raised the research to a new level. Treatment now centers on three approaches: preserving the intact neurons; restoring the surviving ones to best use their function; and--most difficult and most promisingly--regenerating new neural connections.
To preserve the neurons, researchers have to catch them before decay. Stroke research has shown scientists which nerve chemicals flood in to kill nerve cells after a trauma, and they now have one drug to block the process and others on the way. Dr. Dennis Choi at Washington University in St. Louis, Missouri, studies nerve death in stroke victims. He says, "While we can't do very much about neurons that die because they are mechanically destroyed by the impact, we can do quite a bit to prevent cells from dying in the ripple effect. We have a good sense of the cascade that destroys nerves after impact, and there is a lot of commonality between the brain and the spinal cord in this respect. Many of the same approaches that work in the brain work in the spinal cord."
At Young's center at N.Y.U., other drug treatments for the early stages of spinal cord-injury are being investigated. The goal is to block the destructive secondary effects that destroy nerve fibers and sever their connections to muscle. The most promising approaches to date include blocking the receptors on cells for the neurotransmitter glutamate, a chemical that conducts nerve messages. Excess glutamate is toxic to cells; the overexcited neurons eventually short-circuit because of the overload. Once nerve cells begin to die, they trigger the destructive cascade that Choi refers to, often destroying healthy as well as damaged cells. Another approach is to clamp down on the calcium flood that accompanies dying nerve cells by protecting the cells with chemical blockers that reject calcium. Many of these approaches are being tested in stroke patients, and if they can protect the nerves in the brain after a stroke, they will be tested on spinal-cord-injury patients.