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, January 8, 2019

Spreading depolarization A mysterious and deadly mediator of acute brain injury, hemorrhage

You'll have to ask your doctor what protocol they are using to prevent this problem from the  cascade of death. Since they likely have no protocols ask what researchers they are working with to solve this problem. No researcher contact, call the stroke hospital president and ask why incompetency is allowed in their hospital. Delayed cerebral ischemia is too milquetoast a term to suggest immediate critical response needed, the hemorrhage cascade of death should be used since it implies extreme urgency.

Spreading depolarization A mysterious and deadly mediator of acute brain injury


Stephan A. Mayer, Raimund Helbok

Studies in subarachnoid hemorrhage (SAH) have traditionally focused on delayed secondary ischemic injury due to vasospasm, but more recently, attention has turned to early brain injury (EBI) in patients with poor-grade injury. The predictable and delayed nature of secondary brain injury makes SAH a unique illness. Large vessel arterial vasospasm occurs in approximately 70% of patients starting 3 to 5 days after the initial hemorrhage, peaking at 5 to 10 days, then slowly resolving over the following week or two.1 Delayed cerebral ischemia (DCI), defined as infarction, neurologic deterioration, or both from large vessel vasospasm occurs in about 20% of patients with SAH. Interventions and clinical investigation have long focused on DCI. Large trials have failed to improve long-term neurologic outcome despite ameliorating vasospasm.2 This has led to novel concepts of DCI pathophysiology, including microthrombosis, neuroinflammation, and cortical spreading depolarization (SD).1

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