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.

Showing posts with label thrombus. Show all posts
Showing posts with label thrombus. Show all posts

Tuesday, April 11, 2017

Shear sensitive nanocapsule drug release for site specific inhibition of occlusive thrombus formation

Maybe your doctor can use this to remove the blood clots inside your blood vessels. 
http://www.docguide.com/shear-sensitive-nanocapsule-drug-release-site-specific-inhibition-occlusive-thrombus-formation?

Molloy C, Yao Y, Kammoun H, Bonnard T, Hoefer T, Alt K, Tovar-Lopez F, Rosengarten G, Ramsland P, van der Meer A, van den Berg A, Murphy A, Hagemeyer C, Peter K, Westein E; Journal of Thrombosis and Haemostasis (Mar 2017)

BACKGROUND Myocardial infarction and stroke remain the leading causes of mortality and morbidity. The major limitation of current antiplatelet therapy is that their effective concentrations are limited due to bleeding complications. Targeted delivery of antiplatelet drug to sites of thrombosis would overcome these limitations.
OBJECTIVES Here, we have exploited a key biomechanical feature specific to thrombosis; significantly increased blood shear stress due to a reduction in the lumen of the vessel, to achieve site directed delivery of the clinically used antiplatelet agent eptifibatide using shear-sensitive phosphatidylcholine based nanocapsules.
METHODS 2.8x10(12) PC based nanocapsules with high dose encapsulated eptifibatide were introduced in microfluidic blood perfusion assays and in in vivo models of thrombosis and tail bleeding.
RESULTS Shear-triggered nanocapsule delivery of eptifibatide inhibited in vitro thrombus formation selectively under stenotic and high shear flow conditions above 1,000 s(-1) shear rate while leaving thrombus formation under physiological shear rates unaffected. Thrombosis was effectively prevented in in vivo models of vessel wall damage. Importantly, mice infused with shear sensitive antiplatelet nanocapsules did not display prolonged bleeding times.
CONCLUSIONS Targeted delivery of eptifibatide by shear-sensitive nanocapsules offers site specific antiplatelet potential and may form a basis for developing more potent and safer antiplatelet drugs. This article is protected by copyright. All rights reserved.

Tuesday, March 14, 2017

Shear sensitive nanocapsule drug release for site specific inhibition of occlusive thrombus formation

I must be missing something here, if the artery is blocked then blood wouldn't be flowing there resulting in no shear forces at all.

Shear sensitive nanocapsule drug release for site specific inhibition of occlusive thrombus formation

Molloy C, Yao Y, Kammoun H, Bonnard T, Hoefer T, Alt K, Tovar-Lopez F, Rosengarten G, Ramsland P, van der Meer A, van den Berg A, Murphy A, Hagemeyer C, Peter K, Westein E; Journal of Thrombosis and Haemostasis (Mar 2017)

BACKGROUND Myocardial infarction and stroke remain the leading causes of mortality and morbidity. The major limitation of current antiplatelet therapy is that their effective concentrations are limited due to bleeding complications. Targeted delivery of antiplatelet drug to sites of thrombosis would overcome these limitations.
OBJECTIVES Here, we have exploited a key biomechanical feature specific to thrombosis; significantly increased blood shear stress due to a reduction in the lumen of the vessel, to achieve site directed delivery of the clinically used antiplatelet agent eptifibatide using shear-sensitive phosphatidylcholine based nanocapsules.
METHODS 2.8x10(12) PC based nanocapsules with high dose encapsulated eptifibatide were introduced in microfluidic blood perfusion assays and in in vivo models of thrombosis and tail bleeding.
RESULTS Shear-triggered nanocapsule delivery of eptifibatide inhibited in vitro thrombus formation selectively under stenotic and high shear flow conditions above 1,000 s(-1) shear rate while leaving thrombus formation under physiological shear rates unaffected. Thrombosis was effectively prevented in in vivo models of vessel wall damage. Importantly, mice infused with shear sensitive antiplatelet nanocapsules did not display prolonged bleeding times.
CONCLUSIONS Targeted delivery of eptifibatide by shear-sensitive nanocapsules offers site specific antiplatelet potential and may form a basis for developing more potent and safer antiplatelet drugs. This article is protected by copyright. All rights reserved.

Tuesday, January 24, 2017

Is Unexplained Early Neurological Deterioration After Intravenous Thrombolysis Associated With Thrombus Extension?

God, are these people that unknowing/incompetent that they have no fucking clue about these  5 causes of neuronal cascade of death in the first week?

Is Unexplained Early Neurological Deterioration After Intravenous Thrombolysis Associated With Thrombus Extension

Pierre Seners, Robert Hurford, Marie Tisserand, Guillaume Turc, Laurence Legrand, Olivier Naggara, Jean-Louis Mas, Catherine Oppenheim, Jean-Claude Baron

This article requires a subscription to view the full text. If you have a subscription you may use the login form below to view the article. Access to this article can also be purchased.


Abstract

Background and Purpose—Early neurological deterioration (END) after anterior circulation stroke is strongly associated with poor outcome. Apart from straightforward causes, such as intracerebral hemorrhage and malignant edema, the mechanism of END occurring after intravenous thrombolysis remains unclear(Then you are completely incompetent in not keeping up with research) in most instances. We tested the hypothesis that unexplained END is associated with thrombus extension.
Methods—From our database of consecutively thrombolysed patients, we identified anterior circulation stroke patients who had both admission and 24-hour T2* magnetic resonance imaging, visible occlusion on admission magnetic resonance angiography and no recanalization on 24-hour magnetic resonance angiography. END was defined as ≥4 National Institutes of Health Stroke Scale–point deterioration on 24-hour clinical assessment and unexplained END as END without clear cause. The incidence of susceptibility vessel sign extension on T2* imaging, defined as any new occurrence or extension of susceptibility vessel sign from admission to 24-hour follow-up magnetic resonance, was compared between patients with unexplained END and those without END.
Results—Of 120 eligible patients for the present study, 22 experienced unexplained END. Susceptibility vessel sign extension was present in 41 (34%) patients and was significantly more frequent in the unexplained END than in the no-END group (59% versus 29%, respectively; adjusted odds ratio=3.96; 95% confidence interval, 1.25–12.53; P=0.02).
Conclusions—In this study, unexplained END occurring after thrombolysis was independently associated with susceptibility vessel sign extension, suggesting in situ thrombus extension or re-embolization. These findings strengthen the need to further investigate early post-thrombolysis administration of antithrombotics to reduce the risk of this ominous clinical event.

Monday, July 25, 2016

Clots, Collaterals, and the Intracranial Arterial Tree

But you are not even discussing the neuronal cascade of death by these 5 causes in the first week. You're NOT SOLVING STROKE AT ALL! What are you doing in stroke research then?
DO YOU NOT KNOW ABOUT THIS?

Clots, Collaterals, and the Intracranial Arterial Tree


  1. Mayank Goyal, MD
+ Author Affiliations
  1. From the Departments of Clinical Neurosciences (B.K.M., M.G.), Radiology (B.K.M., M.G.), Community Health Sciences (B.K.M., M.G.), and Medicine (B.K.M., M.G.), Cumming School of Medicine, University of Calgary, Calgary, Canada; and The Hotchkiss Brain Institute, Calgary, Canada (B.K.M.).
  1. Correspondence to Mayank Goyal, MD, Department of Radiology, Seaman Family MR Research Centre, Foothills Medical Centre, 1403 – 29th St NW, Calgary AB T2N 2T9, Canada. E-mail mgoyal@ucalgary.ca
Key Words:
See related article, p 2061.
Acute ischemic stroke is a story of two parts; a thrombus blocks anterograde blood flow within the intracranial arterial tree while tiny vessels called collaterals sustain the brain until the thrombus is cleared. The location, size, and type of thrombus along with the degree and extent of collaterals likely determine the patient’s clinical symptoms, the likelihood of treatment success and the patient’s prognosis. A major focus of acute stroke research has been to image and measure various thrombus and collateral characteristics that help predict patient outcomes.(Shit, stop predicting and start solving.)
In vitro studies show that larger clots are less likely to lyse with thrombolytic agents, whereas clots with more surface area exposed to flowing blood are more likely to lyse early.1 This information can be used to create a theoretical framework for thrombus lysis within the intracranial arterial tree.2 Thrombi in proximal arteries such as the internal carotid or the M1 segment of the middle cerebral artery are likely to have greater volume than thrombi in smaller more distal arteries. Independent of thrombus volume, longer thrombi within the cylindrical framework of the intracranial arterial tree are likely to have less relative surface area (at the proximal and distal ends) exposed to blood flow. Poor collateral status is likely to result in less blood flow at the distal end of any thrombi within the arterial tree.2 Less number of arterial branches at the proximal and distal ends of thrombi are more likely to result in stasis …