Deans' stroke musings: Brainstem discovered as important relay site after stroke

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.

Wednesday, March 12, 2014

Brainstem discovered as important relay site after stroke

Don't just tell me it is important, find out how to use it to help recovery. Damn, don't people think at all?
Article here:
http://www.sciencedaily.com/releases/2014/02/140225193233.htm
Abstract here:
Sprouting of Brainstem–Spinal Tracts in Response to Unilateral Motor Cortex Stroke in Mice

Lukas C. Bachmann¹,²,*,
Nicolas T. Lindau¹,²,*,
Petra Felder¹,², and
Martin E. Schwab¹,²

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Author contributions: L.C.B., N.T.L., and M.E.S. designed research; L.C.B., N.T.L., and P.F. performed research; L.C.B. and N.T.L. contributed unpublished reagents/analytic tools; L.C.B., N.T.L., and P.F. analyzed data; L.C.B., N.T.L., and M.E.S. wrote the paper.
↵*L.C.B. and N.T.L. contributed equally to this work.

The Journal of Neuroscience, 26 February 2014, 34(9): 3378-3389; doi: 10.1523/JNEUROSCI.4384-13.2014

Abstract

After a stroke to the motor cortex, sprouting of spared contralateral corticospinal fibers into the affected hemicord is one mechanism thought to mediate functional recovery. Little is known, however, about the role of the phylogenetically old, functionally very important brainstem–spinal systems. Adult mice were subjected to a unilateral photothrombotic stroke of the right motor cortex ablating 90% of the cross-projecting corticospinal cells. Unilateral retrograde tracing from the left cervical spinal hemicord devoid of its corticospinal input revealed widespread plastic responses in different brainstem nuclei 4 weeks after stroke. Whereas some nuclei showed no change or a decrease of their spinal projections, several parts of the medullary reticular formation as well as the spinally projecting raphe nuclei increased their projections to the cortically denervated cervical hemicord by 1.2- to 1.6-fold. The terminal density of corticobulbar fibers from the intact, contralesional cortex, which itself formed a fivefold expanded connection to the ipsilateral spinal cord, increased up to 1.6-fold specifically in these plastic, caudal medullary nuclei. A second stroke, ablating the originally spared motor cortex, resulted in the reappearance of the deficits that had partially recovered after the initial right-sided stroke, suggesting dependence of recovered function on the spared cortical hemisphere and its direct corticospinal and indirect corticobulbospinal connections.