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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