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.

Tuesday, September 22, 2020

Early neurological deterioration following thrombolysis for minor stroke with isolated internal carotid artery occlusion

 

And just WHY THE FUCK are you predicting disability rather than producing recovery? Useless.

 The latest here:

Early neurological deterioration following thrombolysis for minor stroke with isolated internal carotid artery occlusion

First published: 21 September 2020
https://doi.org/10.1111/ene.14541

This article has been accepted for publication and undergone full peer review but has not been through the copyediting, typesetting, pagination and proofreading process, which may lead to differences between this version and the Version of Record. Please cite this article as doi:10.1111/ene.14541

Abstract

Background

Better understanding the incidence, predictors and mechanisms of early neurological deterioration (END) following intravenous thrombolysis (IVT) for acute stroke with mild symptoms and isolated internal carotid artery occlusion (iICAo) may inform therapeutic decisions.

Methods

From a multicenter retrospective database we extracted all patients with both NIHSS<6 and iICAo (i.e. not involving the Willis circle) on admission imaging, intended for IVT alone. END was defined as ≥4 NIHSS points increase within 24hrs. END and no‐END patients were compared for i) pre‐treatment clinical and imaging variables, and ii) occurrence of intracranial occlusion, carotid recanalization and parenchymal hemorrhage on follow‐up imaging.

Results

Seventy‐four patients were included, among whom 22 (30%) patients experienced END. Among pre‐treatment variables, supra‐bulbar carotid occlusion was the only admission predictor of END following stepwise variable selection (OR=4.0; 95%CI 1.3‐12.2; P=0.015). On follow‐up imaging, there was no instance of parenchymal hemorrhage but an intracranial occlusion was now present in 76% vs. 0% of END and no‐END patients, respectively (P<0.001), and there was a trend towards higher carotid recanalization rate in END patients (29% vs. 9%, P=0.07). As compared to no‐END, END was strongly associated with poor 3‐month outcome.

Conclusions

END is a frequent and highly deleterious event after IVT for minor stroke with iICAo, and is of thrombo‐embolic origin in 3 out of 4 patients. The strong association with iICAo site –largely a function of underlying stroke etiology– may point to a different response of the thrombus to IVT. These findings suggest END may be preventable in this setting.

 
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