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.

Saturday, October 8, 2016

Levosimendan, a new therapeutic approach to prevent delayed cerebral vasospasm after subarachnoid hemorrhage?

Bet this will still take decades before it is rolled out for general use. Our fucking failures of stroke associations will not lift a finger to get this into use faster to actually help stroke survivors. We have NO fucking stroke leadership. It isn't even a BHAG.
http://www.mdlinx.com/internal-medicine/medical-news-article/2016/10/03/levosimendandcvsdelayed-cerebral-vasospasmtakotsubo-cardiomyopathysubarachnoid-hemorrhagesahet-a/6859528/?
Acta Neurochirurgica, 10/03/2016
The consequences of this study exhibited that, after experimental–induced delayed cerebral vasospasm (dCVS), levosimendan appears to restore the well–known impaired function of the vasorelaxant ET–(B1) receptor. Levosimendan additionally reversed the prostaglandin F2alpha (PGF)–induced contraction dose–dependently, and both of these mechanisms could be used for antagonizing dCVS in patients suffering subarachnoid hemorrhage (SAH). Also, levosimendan could even be utilized in treating patients developing takotsubo cardiomyopathy.
Go to PubMed Go to Abstract Print Article Summary Cat 2 CME Report

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