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, September 23, 2011

Immunoglobulins promote remyelination in the central nervous system

So for damage to the white matter this might help.
http://onlinelibrary.wiley.com/doi/10.1002/ana.410270104/abstract

Abstract

Remyelination of central nervous system axons was promoted by systemic injection of serum immunoglobulin G (IgG) from donor mice hyperimmunized with homogenized spinal cord. In SJL/J mice infected with Theiler's virus, primary demyelination and inflammation in the spinal cord were extensive. Following treatment with IgG to spinal cord homogenate, new myelin synthesis as measured by quantitative morphometry increased sixfold. Cells in areas of remyelination that incorporated [3H]thymidine did not express differentiation markers of macrophages, oligodendrocytes, or astrocytes but were identified by electron microscopic autoradiography as progenitor glial cells. These findings raise the possibility that IgG secreted in demyelination lesions might have the protential to promote myelin repair.

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