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.

Tuesday, November 21, 2017

Chapter 20 – Animal Models of Ischemic Stroke Versus Clinical Stroke: Comparison of Infarct Size, Cause, Location, Study Design, and Efficacy of Experimental Therapies

You'll have to ask your doctor if this analysis covered Dr. Michael Tymianski of the Toronto Western Hospital Research Institute in Canada referencing 1000+ failed neuroprotective clinical trials.
https://www.sciencedirect.com/science/article/pii/B9780128094686000206

Abstract

A quantitative and qualitative comparison of contemporary neuroprotection and thrombolytic stroke trials and their preclinical animal counterparts has been undertaken, with metaanalysis [DerSimonian, R., Laird, N., 1986. Metaanalysis in clinical trials. Control. Clin. Trials 7 (3), 177–188.] used to evaluate imaging and histological outcomes.
Results from 35 clinical trials including 5,532 patients were compared with data from 3,145 preclinical acute-stroke experiments in 45,476 animals. While clinical trials tended to be of higher methodological quality and have larger sample sizes than animal experiments (71 patients vs. 7 animals per group), both were similarly underpowered owing to the greater variability in human stroke (average standard deviation of mean in humans 99% vs. 30% in animals). Proportionally, animal infarcts were almost 4 times larger than human infarcts in untreated control groups (27% vs. 8% of the hemisphere) although there was considerable variability in size owing to comorbidities and stroke type. Eighty-six percent of animal studies and 54% of clinical trials reported smaller infarcts in groups receiving treatment, with 41% of clinical trials reporting an improvement in the prespecified hypothesis. Animal experiments were not effective in predicting individual trial results, nor the level of neuroprotection, however, there was a fair agreement between the direction of the animal and clinical outcomes when looking at the overall direction of drug outcome. As a drug-screening tool, experimental stroke studies need refinement. Rational frameworks for translational research will help.

Keywords

  • animal models;
  • cerebral ischemia;
  • focal ischemia;
  • infarct size;
  • metaanalysis;
  • neuroprotection;
  • stroke;
  • thrombolysis
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