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Damage to the brain from a stroke often causes loss of arm and leg movement. As this ScienCentral News video reports, brain researchers have found a way to make damaged nerve cells in the brain re-grow after a stroke, and restore movement to paralyzed limbs.
Life Beyond Stroke
In 2001, a massive stroke left Pete Cornelis all but paralyzed – robbing him of his passion for painting, as well as everyday things like walking and eating. "The only thing I could move on my entire body was my two fingers," he recalls.
But thanks to his treatment at The Neurological Institute of New York, part of Columbia University Medical Center, followed by years of hard work, perseverance and extensive physical therapy, Cornelis managed to regain almost all of his lost movement. "I was surprised by how much I had to relearn," he ays. But, "it is absolutely possible to retrain you brain, to re-wire it, and have it learn what the old [damaged brain] parts used to do." His brain had to slowly work to grow new nerve cells to replace those damaged by the stroke - essentially re-wiring some areas of his brain to compensate for those that were basically dead and could not be revived.
When a stroke occurs, blood flow to part of the brain is interrupted when a blood vessel becomes damaged or blocked. The blood normally brings oxygen and nutrients that the brain cells in the immediate area need to survive. Without the blood the brain cells begin to die and stroke victims lose the functions that were controlled by those brain cells. About 80% of all strokes are ischemic, caused by a blood clot that blocks a blood vessel or artery in the brain. The other 20% are caused by a weakened blood vessel that breaks and bleeds into the brain. This is known as hemorrhagic stroke, and is often fatal. Around 600,000 new strokes, or "brain attacks" are reported each year.
The power of rejuvenation
If Cornelis had been much younger, his brain might have coped better with the damage. In the developing systems of young people and other animals, the central nervous system (CNS), which consists of around ten billion nerve cells, have the ability to spontaneously grow new nerve cell connections. "So there's really no blockade to new growth in the young developing system," says neurologist Wendy Kartje from the Hines Veterans Administration Hospital in Illinois. But, when these young animals grow up and their nervous systems mature, this spontaneous re-growth no longer occurs – something is blocking it. "We know that adults have the same capacity to re-grow, it's just that they're being stopped from re-growing," she says.
The antibody (red) blocks NOGO-A (green) from binding to receptors on the nerve cell.
In recent years, an international team of brain researchers, led by neurologist Martin Schwab, has discovered that a protein called "Nogo-A" inhibits the re-growth and repair of injured nerve cells of the brain and spinal cord in adults. Nogo-A appears to be one of the stabilizers that come into play after development of the central nervous system has finished – when all the nerve fibers have grown to their places, made their appropriate connections, and the whole network is in a functional mature state. "NOGO-A is one of the major inhibitors to new growth, there are others but, NOGO appears to be one of the major ones," Kartje explains.
In tests on stroke-damaged rats Kartje and her research team used a very specific antibody, an immune-system protein, to stop NOGO-A from binding to receptors on nerve cells. Without the inhibitory affect of NOGO-A, the injured nerve cells were able to re-grow, restoring lost movement to the front paws of the rats. "For the first time really we know that there is hope for people who have been disabled from stroke," says Kartje.
As she explained at the 2004 meeting of The American Society for Neurochemistry in New York City, they initially trained the rats to perform highly-skilled tasks, such as reaching through a small hole for food and walking along the rungs of a ladder, which required precise forelimb movement and coordination. A stroke-like injury in either the left or the right side of the sensory-motor cortex – the area at the top of the brain that controls conscious body movement – left the rats with paralysis of the paws on one side, and unable to do the tasks.
Ladder-rung walking test for leg movement. image: Martin Schwab
A week after the stroke, the rats began the two-week antibody treatment to block NOGO-A. "We're giving it one week after the stroke, which gives us a lot of time in the clinical world to get things organized and set up and to actually get therapy to the patient," Kartje explains. At the end of the treatment the researchers began continual testing the rats on their tasks. "By five weeks after the stroke, and after their treatment, basically they begin to dramatically improve," she says. "And we've looked at the connections in the brain, and it's because of reorganization. So, new brain connections are actually formed."
Although Kartje's team was only testing the therapy in the part of the brain that controls sensory movement – an area commonly affected by stroke – "More than likely, this kind of therapy could even be useful for other types of stroke in other parts of the brain," says Kartje, helping to restore lost speech and vision.
The big question now is how long after a stroke would this kind of therapy work? Something Kartje and her colleagues are working on now. "If it is effective, say months after a stroke in the rodent, I would expect that in humans it could be effective for quite a while after stroke, and therefore there is a lot of hope to use this patients that have been disabled for quite a while."
Since his recovery, Pete Cornelis has set up the "Hope 4 Stroke Foundation" to provide support for stroke sufferers and their families, and in particular for stroke victims without insurance to pay for the kind of treatment he was lucky enough to have received.