Silver said the medical community also assumed that the cut axon tips died when they hit the scar wall. In prior research in his lab by his graduate student, Tom, it was discovered that axons are alive and continue to attempt to grow for years. Silver describes them as "trucks stuck in mud going no where." It also explains why some people gain some movement back or come out of comas after many years as the nerve fibers sprout through weakened or remodeled areas of the scar.
About 16 years ago, Silver also made another find that proteoglycans, a sugary protein, is present at the site of spinal cord lesions. He also knew that a particular enzyme from the bacteria Proteus vulgaris, called chondroitinase, might dismantle the proteoglycans by clipping their sugar branches, thereby preventing the scar wall from building.
In a National Institutes of Health-supported animal study, 12 rats had spinal injuries at the cervical level 3 (C3) that resulted in impaired motor functions to their right side limbs. The animals had trouble moving, climbing or grooming.
Combining the old with the new, the researchers grafted a 1.5 centimeter piece of the tibial branch of he sciatic nerve to the C3 area of the spinal cord and allowed the nerve fibers to grow and regenerate over three weeks. .
At approximately two and a half weeks into the new nerve growth, Houle implanted a small pump that delivered a steady dose of chondroitinase to a new incision site near C5 where the researchers hoped to reconnect the other end of the bridge to the spinal cord, but also prevent further scarring. They also primed the newly re-grown axons for rapid regeneration by clipping
Source:Case Western Reserve University