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, July 5, 2013

Axonal Remodeling of the Corticospinal Tract in the Spinal Cord Contributes to Voluntary Motor Recovery After Stroke in Adult Mice

Read the conclusion paragraph and demand to know that means from your neurologist.
http://stroke.ahajournals.org/content/44/7/1951.abstract

Abstract

Background and Purpose—We sought to demonstrate the contribution of axonal remodeling of the corticospinal tract (CST) in the spinal cord to functional outcome after stroke.
Methods—Bilateral pyramidotomy (BPT) or sham-BPT was performed in mice with transgenic yellow fluorescent protein labeling in the CST subjected to middle cerebral artery occlusion (MCAo). Foot-fault and single pellet reaching tests were performed 3 days after MCAo and weekly thereafter. Mice were euthanized at day 14 or 28 after stroke. Immunofluorescent staining for growth-associated protein-43 and Synaptophysin was performed on cervical sections.
Results—Functional improvements were evident during the initial 14 days in both MCAo-sham-BPT and MCAo-BPT mice (P<0.01, versus day 3). Progressive recovery was present during the subsequent 14 days in MCAo-sham-BPT mice (P<0.001, versus day 14) but not in MCAo-BPT mice. In the stroke-affected cervical gray matter of MCAo-sham-BPT mice, growth-associated protein-43-Cy3 staining on CST axons were significantly increased at day 14 after stroke compared with normal mice (P<0.001), and CST axonal density and Synaptophysin-Cy3 staining of CST-yellow fluorescent protein axonal terminals were significantly increased at day 28 compared with day 14 after MCAo (P<0.001).
Conclusions—Our data demonstrate that voluntary motor recovery is associated with CST axonal outgrowth and synaptic formation in the denervated side of the spinal gray matter during the later phase after stroke, suggesting that the CST axonal plasticity in the spinal cord contributes to neurological recovery.

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