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.

Monday, June 7, 2021

Infarct Growth despite Successful Endovascular Reperfusion in Acute Ischemic Stroke: A Meta-analysis

 REALLY? You somehow missed knowing this neuronal cascade of death  was occurring. And your mentors and senior researchers didn't know about it either? Known since Rockefeller University coined the term back in 2009. Neuroprotection is a useless word, it gives no sense of urgency needed. When your doctor says; 'We haven't been able to stop the neuronal cascade of death, so billions of neurons will die'. What will be your response? 'Oh well, it's not like you've known about this for decades, have you?' This is appallingly bad research.

Infarct Growth despite Successful Endovascular Reperfusion in Acute Ischemic Stroke: A Meta-analysis

F. Bala, J. Ospel, B. Mulpur, B.J. Kim, J. Yoo, B.K. Menon, M. Goyal, C. Federau, S.-I. Sohn, M.S. Hussain and M.A. Almekhlafi

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Abstract

BACKGROUND: Infarct volume inversely correlates with good recovery in stroke. The magnitude and predictors of infarct growth despite successful reperfusion via endovascular treatment are not known.

PURPOSE: We aimed to summarize the extent of infarct growth in patients with acute stroke who achieved successful reperfusion(Since the infarct was still growing you didn't have a successful reperfusion.) (TICI 2b–3) after endovascular treatment.

DATA SOURCES: We performed a systematic review and meta-analysis by searching MEDLINE and Google Scholar for articles published up to October 31, 2020.

STUDY SELECTION: Studies of >10 patients reporting baseline and post-endovascular treatment infarct volumes on MR imaging were included. Only patients with TICI 2b–3 were included. We calculated infarct growth at a study level as the difference between baseline and follow-up MR imaging infarct volumes.

DATA ANALYSIS: Our search yielded 345 studies, and we included 10 studies reporting on 973 patients having undergone endovascular treatment who achieved successful reperfusion.

DATA SYNTHESIS: The mean baseline infarct volume was 19.5 mL, while the mean final infarct volume was 37.5 mL(This tells us nothing. How many additional neurons died? How many additional miles of connections were destroyed? How many synapses were destroyed?). A TICI 2b reperfusion grade was achieved in 24% of patients, and TICI 2c or 3 in 76%. The pooled mean infarct growth was 14.8 mL (95% CI, 7.9–21.7 mL). Meta-regression showed higher infarct growth in studies that reported higher baseline infarct volumes, higher rates of incomplete reperfusion (modified TICI 2b), and longer onset-to-reperfusion times.

LIMITATIONS: Significant heterogeneity among studies was noted and might be driven by the difference in infarct growth between early- and late-treatment studies.

CONCLUSIONS: These results suggest considerable infarct growth despite successful endovascular treatment reperfusion and call for a faster workflow and the need for specific therapies to limit infarct growth.

 

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