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.

Friday, August 8, 2014

Reperfusion Injury in Stroke

Another issue that your doctor needs to solve to stop the neuronal cascade of death.
One way to solve it is by interrupting the reperfusion after the clot is removed.
Reperfusion Injury in Stroke

Overview

Cerebral hyperperfusion, or reperfusion syndrome, is a rare, but serious, complication following revascularization. Hyperperfusion is defined as a major increase in ipsilateral cerebral blood flow (CBF) that is well above the metabolic demands of the brain tissue. Quantitatively, hyperperfusion is a 100% or greater increase in CBF compared with baseline.[1]
This definition also extends to rapid restoration of normal perfusion pressure, for example, with thrombolytic therapy for acute ischemic stroke. Reperfusion syndrome can occur as a complication of carotid endarterectomy (CEA), intracranial stenting, and even bland cerebral infarction.
The terms hyperperfusion and reperfusion are often used interchangeably. The former implies excessive flow, while the later suggests normalization of flow.[1, 2] Both can result in cerebral injury with similar clinical pictures, which is the reason for the substitution of terms. However, not all patients with hyperperfusion are symptomatic; conversely, patients with only moderate rises in CBF can have devastating outcomes. Therefore, some authors prefer to address this subject as reperfusion syndrome.[2]
When patients are identified and treated early, the prognosis is better and the incidence of intracranial hemorrhage is decreased.[3] Outcomes are dependent on timely recognition and prevention of precipitating factors. Most important is the treatment of hypertension before it can inflict damage in the form of edema or hemorrhage.
The prognosis following hemorrhagic transformation is poor. Mortality in such cases is 36-63%, and 80% of survivors have significant morbidity.[4, 5, 6]
Studies indicate that reperfusion injury is involved directly in the potentiation of stroke damage. Components of the inflammatory response, including cytokine release and leukocyte adhesion, appear to play key roles in these deleterious effects.
Damage to the blood-brain barrier (BBB), an important factor in reperfusion injury, is seen in the image below.

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