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Last Updated: Sunday, 23 November, 2003, 00:47 GMT
Nerve death throes 'wreck spine'
Spinal injuries were simulated in rats
Spinal injuries may be made much worse by a chemical chain reaction set off by even minor damage to nerves.

As the nerves die, they trigger the release of chemicals which kill neighbouring cells.

Scientists from Ohio State University in the US believe that preventing this reaction could reduce the damage suffered by spinal injury patients.

Treatments could prevent long term disability in some patients, they told a neuroscience conference.

The study took a detailed look at exactly what happens when someone suffers a spinal cord injury.

At present, there is very little that medicine can offer to people even in the days following spinal injury which might reduce the damage.

Afterwards, nerve tissue in the spine does not regrow back properly.

While the initial injury can cause severe damage to vital nerve cells, it is only in the days or even weeks that follow the initial injury that the substantial damage is done.

Often the problems caused by these "secondary" injuries are more severe for patients than the initial damage suffered.


Dr Randy Christensen, who led the study, carried out experiments on rats to see which cells were affected, in which order, and to try to identify which body chemicals triggered the problem.

Two chemicals, called glutamate and tumour necrosis factor alpha (TNFa), appear to be to blame.

The latter of these is linked to the body's immune response after injury, while the other is a "neurotransmitter" which helps nerve cells pass on messages.

The researchers injected high concentrations of the chemicals into the previously uninjured spines of the rats.

Many of the cells don't die until long after the initial injury
Dr Randy Christensen, Ohio State University
They found that damage which looked like spinal cord injury began to appear.

Different types of nerve cells were destroyed one after the other leaving large sections of dead tissue.

While the body's natural immune response is designed to speed healing, in this case, it overstimulates the cells, which end up self-destructing.

Dr Christensen said that it might be possible to stop this "secondary" damage, and perhaps improve the lot of spinal injury patients.

"Preventing over-stimulation caused by glutamate and TNFa together may be viable strategy for therapeutic intervention after human spinal cord injury.

"The time course is pretty important, because in spinal cord injury, many of the cells don't die until long after the initial injury."

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