Deans' stroke musings: PATHOLOGY OF ISCHEMIC INFARCTS

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.

Saturday, June 13, 2015

PATHOLOGY OF ISCHEMIC INFARCTS

This course explains what occurs to the exact location of your stroke. I would have appreciated knowing this but my doctor told me nothing about my stroke or recovery. I worried about my brain rotting from the damage. The picture from there is rather gruesome, which probably resembles my brain right now.
http://neuropathology-web.org/chapter2/chapter2bCerebralinfarcts.html
In the first day or so, the infarct appears as a poorly demarcated area of softening.

CT Imaging at this stage may be negative, especially in brain stem infarcts. MRI is much more sensitive. At the peak of edema, the infarct appears hypodense and bright on T2 MRI images. The infarcted tissue becomes sharply demarcated and softens progressively. From the second week onward, it begins to disintegrate and is gradually replaced by a cavity. The size and location of infarcts follows the anatomy of vascular territories.

Microscopical examination in the first 24 to 48 hours reveals anoxic neurons, pallor of staining and vacuolization of the white matter due to unraveling of myelin, and axonal swellings. During the first week, there is a transient inflammatory reaction, especially around blood vessels and in the meninges, due to release of arachidonic and other fatty acids. As the core of the infarct disintegrates, endothelial cells from the periphery proliferate, and capillaries grow into the dead tissue. Neovascularization (which accounts for contrast enhancement) peaks at 2 weeks. Monocytes from the blood stream enter the infarct through damaged vessels. They ingest the products of degradation of neurons and myelin and are transformed into lipid-laden macrophages. Macrophage reaction appears early and peaks at 3-4 weeks. Astrocytes from the surrounding undamaged brain proliferate and form a glial scar around the infarct. This is completed in approximately 2 months. After that, the infarct remains unchanged. With maturation of new capillaries and glial scar formation, the blood brain barrier is once again sealed. Neurons do not regenerate. So, some brain tissue is lost forever.