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.
Originally published24 Oct 2018Stroke. 2018;0:STROKEAHA.118.022015
Abstract
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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