Deans' stroke musings: Molecular control of brain plasticity and repair

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, August 13, 2014

Molecular control of brain plasticity and repair

How is your doctor enabling this post-stroke? 5 years is plenty of time to create a stroke protocol for this. Has your hospital created goals and objectives for neurologists to create stroke protocols within 6 months of research being released? Is your board of directors enforcing adherence to results oriented goals? Does your hospital have any stroke related goals at all? 30 day deaths improved every year? Following Get With the Guidelines or Joint Commission certification are not valid because they are not results oriented.
http://www.ncbi.nlm.nih.gov/pubmed/19660677

Fawcett J.

Author information

Abstract

Recovery of function after damage to the CNS is limited due to the absence of axon regeneration and relatively low levels of plasticity. Plasticity in the CNS can be reactivated in the adult CNS by treatment with chondroitinase ABC, which removes glycosaminoglycan (GAG) chains from chondroitin sulfate proteoglycans (CSPGs). Plasticity in the adult CNS is restricted by perineuronal nets (PNNs) around many neuronal cell bodies and dendrites, which appear at the closure of critical periods and contain several inhibitory CSPGs. Formation of these structures and the turning off of plasticity is triggered by impulse activity in neurons. Expression of a link protein by neurons is the event that triggers the formation of PNNs. Treatment with chondroitinase removes PNNs and other inhibitory influences in the damaged spinal cord and promotes sprouting of new connections. However, promoting plasticity by itself does not necessarily bring back useful behavior; this only happens when useful connections are stabilized and inappropriate connections removed, driven by behavior. Thus after rodent spinal cord injury, combining a daily rehabilitation treatment for skilled paw function with chondroitinase produces much greater recovery than either treatment alone. The rehabilitation must be specific for the behavior that is to be enhanced because non-specific rehabilitation improves locomotor behavior but not skilled paw function. Plasticity-enhancing treatments may therefore open up a window of opportunity for successful rehabilitation.