Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Friday, November 17, 2017

At the Bench-Stroke Recovery: Inducing Spinal Plasticity Amplifies Benefits of Rehabilitative Training and Improves Stroke Recovery

Now we just need human followup. Is your stroke hospital so fucking incompetent that they will do nothing to advance this research to humans?
http://journals.lww.com/neurotodayonline/Fulltext/2017/11160/At_the_Bench_Stroke_Recovery__Inducing_Spinal.7.aspx
Kreimer, Susan
doi: 10.1097/01.NT.0000527322.43736.10
Features
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ARTICLE IN BRIEF

In an animal model of stroke, researchers removed plasticity-inhibiting signals in the spinal cord (via intraspinal injections of the enzyme chondroitinase ABC), which augmented rewiring of circuits connecting the brain to the spinal cord, even weeks after stroke. The researchers proposed that this plasticity can be harnessed by rehabilitative training to significantly promote sensorimotor recovery.
A combination of spinal therapy and rehabilitative training resulted in improved recovery in rats, even 28 days after experimental stroke conditions were induced, according to a study published October 12 in The Journal of Neuroscience.
The investigators amplified spinal plasticity during chronic stroke in male rats via intraspinal injections of chondroitinase ABC (ChABC), an enzyme that has been found to remove plasticity-inhibiting signals in the brain. Injections into the contralesional grey matter of the cervical spinal cord administered 28 days after stroke resulted in significant sprouting of corticospinal axons originating in the peri-infarct cortex.
Without rehabilitative training, ChABC injection during chronic stroke led to moderate improvements of sensorimotor deficits, said Ian R. Winship, PhD, a study author and associate professor and director of the neurochemical research unit at the University of Alberta's department of psychiatry in Edmonton, Alberta in Canada. But combined with the spinal therapy, rehabilitative training during chronic stroke was much more effective.
“These data suggest that the permanent disability affecting millions of individuals living with the chronic effects of stroke may be treatable with spinal therapy and rehabilitation initiated even months or years after the stroke,” the study authors wrote. “Our data also emphasize that inducing a state of plasticity is not sufficient to induce recovery, and that combining such therapies with rehabilitative therapy is required for optimal recovery.”
After inducing initial ischemic injury in the rats via photothrombosis, investigators tested their hypothesis that promoting plasticity in the spinal cord during chronic stroke could spur advances in recovery from persistent sensorimotor impairment. Sprouting of spared corticospinal tract axons in the contralesional spinal cord has a major impact on sensorimotor recovery, they noted, but this structural plasticity is limited to the first few weeks after stroke.
“The major drawback of the current approach is that injection of the enzyme only extends a certain distance and acts for a finite period of time,” Dr. Winship said. “In a human, we need the enzyme to be active over a much larger region,” he said, because “the spinal cord is so much bigger in human than in a rat.”
“Our findings strongly suggest that such a treatment could reduce disability due to stroke. The next question is, what would actually be required to undertake this approach in humans?” Dr. Winship told Neurology Today.
He acknowledged that “probably a different delivery system would be required for humans. One solution may be to employ viral vectors, which present a way to genetically express the same enzyme in tissue rather than injecting it directly,” Dr. Winship said. “A viral delivery system would allow for longer expression and greater spread within the spinal cord, and therefore, could be safer and possibly effective in larger animals such as dogs as well as humans.”
“We can do very similar injection procedures without damaging the spinal cord, without inducing any kind of injury, but we would need a system like one of these vectors, if the drug is going to trying to strengthen the wiring between the brain and the spinal cord,” he said.

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