Deans' stroke musings

Changing stroke rehab and research worldwide now.Time is Brain!Just think of all the trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 493 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:

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's quite disgusting that this information is not available from every stroke association and doctors group.
My back ground story is here:

Tuesday, January 3, 2017

Collateral Flow and White Matter Disease in Patients with Internal Carotid Artery Occlusion

I really question if there is any understanding of how carotid occlusion works and whether it leads to a stroke. My right carotid artery is fully occluded(closed up) and that is a good thing, I shouldn't have to worry about a stroke from that artery anymore. The closure of the artery is not the problem, if blood is still flowing thru it is the possible problem, a piece of the occlusion could break off and lodge in the brain causing a stroke. If your Circle of Willis is complete then you are getting enough blood to your brain even if some of the arteries feeding it are closed(2 vertebral and 2 carotid).

Ishikawa M, Sugawara H, Nagai M, Kusaka G, Tanaka Y, Naritaka H; European Neurology 77 (1-2), 56-65 (Dec 2016)

BACKGROUND When an internal carotid artery (ICA) occludes, a patient may develop cerebral infarction (CI). We investigated whether CI caused by ICA occlusion (ICAO) is associated with collateral flow through the anterior and posterior communicating arteries (ACoA and PCoA).
METHODS In 100 patients with ICAO, we investigated CI and white matter disease by performing an MRI and the anatomy of the ACoA and PCoA were investigated by performing magnetic resonance angiography. All patients were divided into the symptomatic CI group or the no-CI group. The collateral flow pathway was estimated by the anterior cerebral artery (ACA)-PCoA score and the collateral flow volume after ICAO was estimated by the middle cerebral artery (MCA) flow score, based on how well the MCA was visualized.
RESULTS Of 100 patients with ICAO, the symptomatic CI group included 36 patients. ACA-PCoA score and white matter disease grades were significantly higher in the CI group (indicating poor collateral flow). More than 80% of patients with an ACA-PCoA score of 4 (poor collateral) experienced symptomatic CI. Thirty-one symptomatic CI patients (86%) had an MCA flow score of 1 or 2 (decreased MCA flow).
CONCLUSION The ACA-PCoA score and white matter disease grade may suggest an increased risk of CI following ICAO.

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