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, 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.
DO YOU NOT KNOW ABOUT THIS?
http://stroke.ahajournals.org/content/47/8/1972.extract?etoc 
  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 …
 

No comments:

Post a Comment