Factors influencing infarct growth including collateral status assessed using computed tomography in acute stroke patients with large artery occlusion

Will you stop trying to predict stroke severity and just simply stop the 5 causes of the neuronal cascade of death in the first week that would result in vastly less dead and damaged neurons. This is pretty much useless for survivor recovery to 100%. I'm sure there are more than these 5 causes but since I don't have minions or a stroke association to add the additional ones I've found, you'll just have to deal with your incompetent doctor not knowing of these and having nothing to stop that neuronal cascade of death. Hope you are pleased with your doctors' service.  My next stroke will be a screaming match with my stroke 'professionals'. 'What did you do 1/5/10 years ago when your patients did not get to 100% recovery?' 'If you did nothing, I want a new doctor, you're fired!'  Doctors who depend on collaterals for YOU to have a less damaging stroke are worthless.  Doctors can control the neuronal cascade of death if they were responsible and smart enough a decade ago to enlist researchers to solve that problem. Not smart enough or not responsible, YOU are the recipient of that incompetency, vastly more dead and damaged neurons than should have occurred. In my 90 minutes before tPA blew out my clot.

In each minute,
1.9 million neurons die
14 billion synapses die
12 km (7.5 miles) of myelinated fibers die
brain ages 3.6 years each hour without treatment

Day 1,: first 90 minutes:
171 million dead neurons 
1.260 trillion dead synapses
675 miles of dead myelinated fibers
Brain aged 5.4 years
Days 2-3; 1/2 the rate of day 1
So 1440 minutes a day * 2days * 950000 = 2,736,000,000  or 2.7 billion  dead neurons
  1440 minutes a day *2days * 7,000,000,000syn = 20,160,000,000,000     20.2 trillion        dead synapses
1440 * 2days * 3.75mi = 10800 mi  dead myelinated fibers
Brain aged - 2 years, a guess

Days 4-7; 1/4 the rate of day 1

So 1440 minutes a day * 4 days * 475000 = 2,736,000,000  or 2.7 billion dead neurons
  1440 minutes a day *4 days * 3,500,000,000syn = 20,160,000,000,000 20.2 trillion    dead synapses
1440 * 4days * 1.875mi = 10800 mi  dead myelinated fibers
Brain aged - 2 years, a guess 
This is one hell of a lot of damage to recover from. Especially since we don't know how to move functions from dead locations to new ones.  Or know how to usefully get neurogenesis to work.
Totals:
5.571 billion dead neurons
4.041260 trillion dead synapses
 22,275 miles dead myelinated fibers
Brain aged -  9.4 years

If I had just lost neurons in those first 90 minutes I would be completely recovered by now.

If your hospital isn't measuring your neuronal death, then nothing will ever improve.  This set of statistics should be required for every hospital to provide.

“What's measured, improves.” So said management legend and author Peter F. Drucker

 

 

 

Factors influencing infarct growth including collateral status assessed using computed tomography in acute stroke patients with large artery occlusion 

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Bin Jiang, Robyn L Ball, Patrik Michel, ...

First Published May 17, 2019 Case Report

https://doi.org/10.1177/1747493019851278

Article information

Abstract

In major ischemic stroke caused by a large artery occlusion, neuronal loss varies considerably across individuals without revascularization. This study aims to identify which patient characteristics are most highly associated with this variability. Demographic and clinical information were retrospectively collected on a registry of 878 patients. Imaging biomarkers including Alberta Stroke Program Early CT score, noncontrast head computed tomography infarct volume, perfusion computed tomography infarct core and penumbra, occlusion site, collateral score, and recanalization status were evaluated on the baseline and early follow-up computed tomography images. Infarct growth rates were calculated by dividing infarct volumes by the time elapsed between the computed tomography scan and the symptom onset. Collateral score was graded into four levels (0, 1, 2, and 3) in comparison with the normal side. Correlation of perfusion computed tomography and noncontrast head computed tomography infarct volumes and infarct growth rates were estimated with the nonparametric Spearman's rank correlation. Conditional inference trees were used to identify the clinical and imaging biomarkers that were most highly associated with the infarct growth rate and modified Rankin Scale at 90 days. Two hundred and thirty-two patients met the inclusion criteria for this study. The median infarct growth rates for perfusion computed tomography and noncontrast head computed tomography were 11.2 and 6.2 ml/log(min) in logarithmic model, and 18.9 and 10.4 ml/h in linear model, respectively. Noncontrast head computed tomography and perfusion computed tomography infarct volumes and infarct growth rates were significantly correlated (rho=0.53; P < 0.001). Collateral status was the strongest predictor for infarct growth rates. For collateral=0, the perfusion computed tomography and noncontrast head computed tomography infarct growth rate were 31.56 and 16.86 ml/log(min), respectively. Patients who had collateral >0 and penumbra volumes>92 ml had the lowest predicted perfusion computed tomography infarct growth rates (6.61 ml/log(min)). Collateral status was closely related to the diversity of infarct growth rates, poor collaterals were associated with a faster infarct growth rates and vice versa.

Keywords Ischemic stroke, computed tomography, perfusion imaging, collateral

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