Changing stroke rehab and research worldwide now.Time is Brain!Just think of all the trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 493 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:

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.
My back ground story is here:http://oc1dean.blogspot.com/2010/11/my-background-story_8.html

Friday, October 26, 2018

Ischemia-Reperfusion Injury After Endovascular Thrombectomy for Ischemic Stroke

But you didn't keep going and determine the neuronal cascade of death injury in the first week. You missed the elephant in the room. You also didn't quantify how many millions of neurons are in that .9 ml area that expanded the lesion. You put that off as inconsequential.  Good, let's take that many millions from your brain and see how you feel about it then. 

Ischemia-Reperfusion Injury After Endovascular Thrombectomy for Ischemic Stroke


Originally publishedStroke. 2018;0:STROKEAHA.118.022015

Background and Purpose—

In experimental models of ischemic stroke, abrupt reperfusion is associated with secondary brain damages, responsible for up to 70% of the final lesion size. Whether this remains true in humans is unknown.

Methods—

Using data from the ASTER randomized trial (Aspiration vs Stent Retriever for Successful Revascularization), we investigated the effect of complete reperfusion (defined as a modified Thrombolysis In Cerebral Infarction 3) after endovascular thrombectomy on early lesion growth as assessed by diffusion-weighted imaging at baseline and 1 day after reperfusion.

Results—

Among 381 patients included in the trial, 35 achieved complete reperfusion, benefited from both baseline and day 1 diffusion-weighted imaging, lacked significant hemorrhagic transformation, and were, therefore, included in the present study. We found that the median growth of the ischemic lesion between baseline and day 1 was only 0.9 mL after complete reperfusion, representing <4% of the mean lesion size. The actual lesion growth occurring after reperfusion is probably even smaller because this lesion growth occurred, at least in part, between baseline imaging and complete reperfusion, as demonstrated by a statistically significant positive correlation between imaging-to-reperfusion time and lesion growth (R2=0.116; P=0.048).

Conclusions—

There is no significant lesion growth after complete reperfusion in most patients. This important discrepancy between clinical and preclinical pathophysiologies should be considered during preclinical evaluation of neuroprotective strategies.

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