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 15, 2011

Psychostimulant Drugs and Neuroplasticity

I don't think this is referring to neuroplasticity in the good sense that we want.
http://www.mdpi.com/1424-8247/4/7/976/pdf
Abstract: Drugs of abuse induce plastic changes in the brain that seem to underlie

addictive phenomena. These plastic changes can be structural (morphological) or synaptic
(biochemical), and most of them take place in the mesolimbic and mesostriatal circuits.
Several addiction-related changes in brain circuits (hypofrontality, sensitization, tolerance)
as well as the outcome of treatment have been visualized in addicts to psychostimulants
using neuroimaging techniques. Repeated exposure to psychostimulants induces
morphological changes such as increase in the number of dendritic spines, changes in the
morphology of dendritic spines, and altered cellular coupling through new gap junctions.
Repeated exposure to psychostimulants also induces various synaptic adaptations, many of
them related to sensitization and neuroplastic processes, that include up- or
down-regulation of D1, D2 and D3 dopamine receptors, changes in subunits of G proteins,
increased adenylyl cyclase activity, cyclic AMP and protein kinase A in the nucleus
accumbens, increased tyrosine hydroxylase enzyme activity, increased calmodulin and
activated CaMKII in the ventral tegmental area, and increased deltaFosB, c-Fos and AP-1
binding proteins. Most of these changes are transient, suggesting that more lasting plastic
brain adaptations should take place. In this context, protein synthesis inhibitors block the
development of sensitization to cocaine, indicating that rearrangement of neural networks
must develop for the long-lasting plasticity required for addiction to occur.
Self-administration studies indicate the importance of glutamate neurotransmission in
neuroplastic changes underlying transition from use to abuse. Finally, plastic changes in
the addicted brain are enhanced and aggravated by neuroinflammation and neurotrophic
disbalance after repeated psychostimulants.

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