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, May 27, 2016

Drug Targeting Blood-Brain Barrier 'Hopeful' in Stroke

Would this be a possible solution to  Inflammatory action leaking through the blood brain barrier. in the neuronal cascade of death? More research needed that will never occur.
http://www.medscape.com/viewarticle/863881?
A possible new treatment for acute ischemic stroke targeting the blood-brain barrier has shown promising results in an early randomized clinical trial.
The drug, imatinib, is a tyrosine kinase inhibitor already available for the treatment of certain cancers.
Initial results in stroke were presented at the recent European Stroke Organisation Conference (ESOC) 2016 by Nils Wahlgren, MD, Karolinska Institute, Stockholm, Sweden.
"We believe our results open up an opportunity for a novel third treatment for acute ischemic stroke to complement thrombolysis and thrombectomy," he concluded.
Professor Wahlgren explained that in experimental models, imatinib has preserved the integrity of the blood-brain barrier, which opens up during ischemic stroke, allowing an influx of inflammatory cells into the brain, and contributes to edema, hemorrhagic transformation, and increased mortality. This effect can be made worse by the use of tissue plasminogen activator (tPA).
"This preliminary randomized study suggested that imatinib is safe and generally well tolerated in ischemic stroke patients treated with IV [intravenous] tPA. The high dose increased neurological scores, and there was a suggestion of improved functional independence and reduced risk of hemorrhagic transformation," Professor Wahlgren stated.
"The effect may be mediated by restoring the integrity of the blood-brain barrier, which can lead to reduced edema and subsequent inflammatory responses," he added.
Commenting for Medscape Medical News, president of the European Stroke Organisation, Valeria Caso, MD, University of Perugia, Italy, said the study was very hopeful.
"These are excellent results in this initial early study. We need to now see what happens in larger trials.
"We have been trying to find agents that improve the efficiency of thrombolysis for many years," she added. "Many neuroprotective drugs have been tried without success, but this agent acts differently — targeting the blood-brain barrier — so it is something novel and it really does look like it could be a light at the end of the tunnel."
I-STROKE
The current study — known as I-STROKE — was conducted to clarify whether imatinib is safe and tolerable in an acute ischemic stroke population and whether there is any indication of reduced hemorrhage and edema and improved neurologic function.
The study involved 60 patients with acute ischemic stroke and a National Institutes of Health Stroke Scale (NIHSS) score of 7 or greater who received tPA within 4.5 hours of symptom onset. They were randomly assigned to one of three doses of imatinib (15 patients each to 400 mg, 600 mg, or 800 mg daily) or no additional treatment (controls) within 1 hour of completion of reperfusion therapy.
Results showed no serious treatment-related adverse events but a few mild reversible effects, such as itching, skin reactions, and nausea and vomiting.
In terms of efficacy, there were 28 hemorrhagic transformations in the study, with no overall difference between the imatinib patients and controls. "However, interestingly there were no transformations at all in the high-dose imatinib group, who were treated within 5 hours of symptom onset," Professor Wahlgren reported.
In terms of neurologic outcomes, there was an improvement in NIHSS scores (from baseline to 90 days) in the control group and then a dose-related stepwise further improvement in imatinib-treated patients, with the highest dose showing the best effect and a significant benefit shown over the control group.

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