Deans' stroke musings

Changing stroke rehab and research worldwide now.Time is Brain!Just think of all the trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 493 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:

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's quite disgusting that this information is not available from every stroke association and doctors group.
My back ground story is here:http://oc1dean.blogspot.com/2010/11/my-background-story_8.html

Thursday, April 6, 2017

Neuroprotective strategies and the underlying molecular basis of cerebrovascular stroke

Whom is going to write this up into a stroke protocol and update the strategy with updated results rather than writing in a journal that will never be read and acted upon by your stroke medical professionals?  A lot of these I haven't even heard about and I consider myself fairly well read on this. That missing dissemination of useful information is a complete failure on the part of our fucking failures of stroke associations.
http://thejns.org/doi/full/10.3171/2017.1.FOCUS16522
Department of Neurosurgery, Clinical Neurosciences Center, University of Utah, Salt Lake City, Utah
ABBREVIATIONS AMPA = α-amino-3-hydroxy-5-methyl-4-isoxazole propionate; ATP = adenosine 5′-triphosphate; GABA = γ-aminobutyric acid; IL = interleukin; mRS = modified Rankin Scale; NIHSS = National Institutes of Health Stroke Scale; NMDA = N-methyl-d-aspartate; RCT = randomized controlled trial; SUR1-TRPM4 = sulfonylurea receptor 1–transient receptor potential melastatin 4; TPA = tissue plasminogen activator.
INCLUDE WHEN CITING DOI: 10.3171/2017.1.FOCUS16522.
Correspondence Min S. Park, Department of Neurosurgery, University of Utah, Clinical Neurosciences Center, 175 North Medical Dr. East, Salt Lake City, UT 84132. email: .

Abstract

Stroke is a leading cause of disability in the US. Although there has been significant progress in the area of medical and surgical thrombolytic technologies, neuroprotective agents to prevent secondary cerebral injury and to minimize disability remain limited. Only limited success has been reported in preclinical and clinical trials evaluating a variety of compounds. In this review, the authors discuss the most up-to-date information regarding the underlying molecular biology of stroke as well as strategies that aim to mitigate this complex signaling cascade. Results of historical research trials involving N-methyl-d-aspartate and α-amino-3-hydroxy-5-methyl-4-isoxazole propionate receptor antagonists, clomethiazole, antioxidants, citicoline, nitric oxide, and immune regulators have laid the groundwork for current progress. In addition, more recent studies involving therapeutic hypothermia, magnesium, albumin, glyburide, uric acid, and a variety of other treatments have provided more options. The use of neuroprotective agents in combination or with existing thrombolytic treatments may be one of many exciting areas of further development. Although past trials of neuroprotective agents in ischemic stroke have been limited, significant insights into mechanisms of stroke, animal models, and trial design have incrementally improved approaches for future therapies.

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