Deans' stroke musings

Changing stroke rehab and research worldwide now.Time is Brain!Just think of all the trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 493 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:

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's quite disgusting that this information is not available from every stroke association and doctors group.
My back ground story is here:

Thursday, January 12, 2017

Recovery after stroke improved with new treatment that creates nerve synapses in the brain, a key factor for learning: Study

Easy application through nasal drops. But I bet NO followup will be done because we have NO stroke leadership or strategy.
Stroke recovery can be improved with a new treatment that creates new nerve synapses – essential for learning – in the brain. Researcher Marcela Pekna explained, “More nerve sprouts and connections between nerve cells are created so that the remaining cells can take over functions that the dead cells once had.” The researchers focused on C3a peptide, which is naturally produced in the body and especially as a result of certain conditions. The researchers administered C3a to mice through nasal drops.
Of the 28 mice with stroke, half received C3a peptide while the other half received a placebo. Those mice treated with C3a recovered much better than the mice on a placebo. Although mice are capable of recovering from stroke even without any therapy, C3a sped up the recovery and enabled them to use their stroke-affected paws more easily and effectively. The effects of the treatment remained four weeks after the completion.
Pekna explained, “Say a stroke kills 10 million brain cells. Newly created cells equal less than one percent of those that died, and how much can that help? The formation of new nerve synapses is what allows a person to learn, for example, to speak or use her hands and legs again.”
Although C3a was successful in promoting stroke recovery it can only be administered through nasal drops. When given orally or intravenously, C3a is inactive. Another issue is the cost of the treatment. C3a is very expensive to produce, so a smaller, cheaper molecule with similar properties needs to be developed. (But with 10 million survivors every year, the quantity needed should easily drive innovation to reduce costs. At least with a great stroke association it would.)
The first and foremost objective of the initial treatment for stroke patients is removing the blood clot. This must be done within the first few hours of experiencing a brain attack to avoid serious damage. Unfortunately, majority of patients arrive too late to the hospital. Combining the emergency treatment with effective rehabilitation therapy can help improve health outcomes and speed up the recovery. Researchers suggest that C3a therapy could even treat other conditions, for example, brain damage after a road accident. Further research is required to explore the potential uses of such treatment.

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