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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