Stroke-Related Disabilities Could be Helped with Regenerated Spinal Cord Fibers

A new study suggests that it may be possible to regenerate spinal cord fibers through treatment for stroke-related disabilities.

A study by researchers at Henry Ford Hospital found "substantial evidence" that a regenerative process involving damaged nerve fibers in the spinal cord could hold the key to better functional recovery by most stroke victims.

These findings offer insight and new hope for stroke victims, which might otherwise lead to long-term disabilities in adults. Although most stroke victims recover various movements in their hands and other body parts, about half are left with weaknesses on one side of their bodies. Even worse, some are permanently disabled. 

Researchers believe that discovering a treatment could improve or restore this lost motor function in stroke patients, which could, in turn, help the brain and nerves repair themselves.

The new Henry Ford research was intended to solve some of the mysteries. It looked at changes in the axons-the fibers, the nerve signal "transmission" lines within the spinal cord that affect voluntary movement after stroke.

Researchers used genetically modified mice in which the axons in the corticospinal tract, a bundle of nerves carrying signals from the brain to the spinal cord, were "stained" with fluorescent matter visible under a powerful microscope.

Mice in the experiment were trained for five days to use their left front paws to retrieve food pellets from a dispenser that's designed to test their dexterity.They were also given a "foot-fault test" to see how well they could walk on an unevenly spaced grid.

Next, the mice were divided into four groups. In one, the carotid arteries were blocked with a suture for one hour, much as a blood clot blocks the flow of blood to the brain in a stroke. After the suture was removed and blood flow was restored, they were given additional surgery to sever the axons of the corticospinal tract. The other groups were either given no surgery or "sham" surgery so they could be used as control groups for comparison to the first.

The single-pellet and foot-fault tests were then given three days after surgery, then weekly for 14 to 28 days to reassess dexterity, the amount of "stroke" damage to voluntary movements and the degree of recovery from the lab-induced "stroke."

"In both behavioral tests used in this study, the mice need to control the paw movement," said Yi Li, M.D., a Henry Ford neuroscientist and lead author of the study. "Severe behavioral deficits of the left forepaw were evident in all of the mice three days after stroke.

"All animals showed significant improvement 14 days after surgery. This recovery progressed in those mice whose axons were not severed. However, in those whose axons had been eliminated, there was no significant recovery."

Researchers believe that in the early stages following a stroke, improvements in voluntary movement can be attributed to reduction in brain swelling due to trauma and other spontaneous repairs, while later improvements result from "neuronal plasticity" - the reorganization or regeneration of nerve cells within the spinal cord in response to changes in the nerve network.

The study is published in the current issue of Stroke.