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.

Sunday, January 14, 2018

Improvement of skilled forelimb use induced by treatment with growth hormone and rehabilitation is dependent on the onset of the treatment after cortical

Benefits found that match human patients. Just when the hell is someone going to write up a stroke protocol on this? I'm guessing never since stroke patients have no say in anything about the stroke medical world. We are just pitiable objects to bring in donations to our fucking failures of stroke associations.

Improvement of skilled forelimb use induced by treatment with growth hormone and rehabilitation is dependent on the onset of the treatment after cortical ablation

Margarita Heredia, PhD1; Jesús Palomero, PhD1; Antonio de la Fuente, MD, PhD1; José María Criado, MD, PhD1; Javier Yajeya, MD, PhD1; Jesús Devesa, MD, PhD2; Pablo Devesa, PhD3; José Luis Vicente-Villardón, PhD4, Adelaida S Riolobos PhD1.
1 Department of Physiology and Pharmacology, Neuroscience Institute of Castilla y León (INCyL), University of Salamanca, Salamanca, Spain. 2 Scientific Direction, Medical Centre Foltra, Teo, Spain. 3 Research and Development. Medical Centre Foltra, Teo, Spain. 4 Department of Statistics, University of Salamanca, Salamanca, Spain.
Abstract
We previously demonstrated that the administration of growth hormone (GH) immediately after severe motor cortex injury, in rats, followed by rehabilitation, improved the functionality of the affected limb and re-expressed nestin in the undamaged contralateral motor cortex.
Here, we analyze whether positive GH effects are restricted to a time window after the cortical injury and if this is dependent on the re-expression of nestin and actin.
Injured animals were treated with GH (0.15 mg/kg/day) or vehicle, at days 7, 14 and 35 after cortical ablation, and rehabilitation was applied at short- and long-term after the lesion. On completion of the long-term rehabilitation, animals were sacrificed and nestin and actin were analyzed by immunoblotting in the undamaged contralateral motor cortex.
Giving GH at days 7 or 35 after the lesion, but not 14 days after it, led to a remarkable improvement in the functionality of the affected paw. The abundance of contralateral nestin and actin re-expression was clearly higher in GH-treated animals; probably because compensatory brain plasticity was established.
GH and immediate rehabilitation are key elements for repairing brain injuries, with the exception of a critical time period; that is, when the GH treatment starts 14 days after the lesion. Our data also indicate that there is not a clear plateau in the recovery from a brain injury. This agrees with our data in human patients.

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