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.

Thursday, July 30, 2015

Experience with the “Good” Limb Induces Aberrant Synaptic Plasticity in the Perilesion Cortex after Stroke

Well if using the 'good' side impairs recovery of the 'bad' side then all survivors are totally fucking screwed in trying to get 100% recovery.  Which to me means we need to stop a lot of the damage in the first place by stopping the neuronal cascade of death.
http://www.jneurosci.org/content/35/22/8604.short?
What is your doctors solution to get around this problem? I don't know is not an ok answer.
  1. Theresa A. Jones2,3
  1. Author contributions: S.Y.K., R.P.A., D.L.A., J.A.K., and T.A.J. designed research; S.Y.K., R.P.A., D.L.A., K.A.T., N.A.D., and T.A.J. performed research; J.A.K. contributed unpublished reagents/analytic tools; S.Y.K., R.P.A., D.L.A., and T.A.J. analyzed data; S.Y.K. and T.A.J. wrote the paper.
  2. *R.P.A. and D.L.A. contributed equally to this work.
  1. The Journal of Neuroscience, 35(22): 8604-8610; doi: 10.1523/JNEUROSCI.0829-15.2015

Abstract

Following unilateral stroke, the contralateral (paretic) body side is often severely impaired, and individuals naturally learn to rely more on the nonparetic body side, which involves learning new skills with it. Such compensatory hyper-reliance on the “good” body side, however, can limit functional improvements of the paretic side. In rats, motor skill training with the nonparetic forelimb (NPT) following a unilateral infarct lessens the efficacy of rehabilitative training, and reduces neuronal activation in perilesion motor cortex. However, the underlying mechanisms remain unclear. In the present study, we investigated how forelimb movement representations and synaptic restructuring in perilesion motor cortex respond to NPT and their relationship with behavioral outcomes. Forelimb representations were diminished as a result of NPT, as revealed with intracortical microstimulation mapping. Using transmission electron microscopy and stereological analyses, we found that densities of axodendritic synapses, especially axo-spinous synapses, as well as multiple synaptic boutons were increased in the perilesion cortex by NPT. The synaptic density was negatively correlated with the functional outcome of the paretic limb, as revealed in reaching performance. Furthermore, in animals with NPT, there was dissociation between astrocytic morphological features and axo-spinous synaptic density in perilesion motor cortex, compared with controls. These findings demonstrate that skill learning with the nonparetic limb following unilateral brain damage results in aberrant synaptogenesis, potentially of transcallosal projections, and this seems to hamper the functionality of the perilesion motor cortex and the paretic forelimb.

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