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:

Monday, January 13, 2014

Drug treatment may be a stroke breakthrough

Aspirin plus fish oil for a hyperacute treatment.  This was written about almost 2 years ago and if we had anything other than craptastic stroke associations clinical trials would be completed. You'll have to challenge your doctor if you have an ischemic stroke as to what is the downside to providing this treatment. I'm sure Dr. Bazan can be found by your doctor with a minute amount of google research.
Thursday, February 02, 2012

Led by Louisiana State University neurologist Dr. Nicolas Bazan, a team of researchers from several institutions has claimed a potential breakthrough in drug treatment to prevent long-term brain damage in those who suffer certain strokes. Bazan directed a study that, using laboratory rats, administered aspirin and an omega-3 essential fatty acid to yield a new protective molecule that can mitigate damage to cells around the area of an ischemic stroke. Ischemic stroke occurs when an arterial blockage denies oxygenated blood to parts of the brain, as opposed to hemorrhagic stroke, which occurs when a vessel bursts inside the brain.
Louisiana State University neurologist Dr. Nicolas Bazan
The results, Bazan said, portend a “novel approach for pharmaceutical intervention.”
Stroke is the fourth-leading cause of death in the United States and the leading cause of newly acquired disability in adulthood. Bazan presented his findings Thursday at the International Stroke Conference, which concludes Friday at the Ernest N. Morial Convention Center in New Orleans.
The study, which was financed by a National Institutes of Health grant, was designed to analyze benefits of neuroprotective agents — long a focus of Bazan’s career — that can help prevent irreversible damage in the stroke-affected area. There is considerable research interest internationally in neuroprotectors as an additional therapy beyond the more developed, widely used thrombolytic therapy or drugs that break up and dissolve the clot itself.
Bazan’s study relied in part on his previous research on the role of omega-3 essential fatty acids in neuroprotection. In the latest discovery, Bazan said the team discovered that aspirin and the omega-3 acid DHA (docosahexaenoic acid) yield in the brain a neuroprotective molecule. Bazan said the synthesis results from how aspirin, a common anti-inflammatory agent, acts on a certain enzyme protein that he described as “evil and angel” in brain chemistry.
In the study with rats, Bazan’s team chemically generated that new molecule outside of the brain. Then, the animal subjects were anesthetized and induced with a middle cerebral artery blockage for two hours. In humans, the middle cerebral artery is the largest artery in the brain and the most commonly affected by stroke. Because it affects such a large portion of the brain, MCA stroke can affect many physical abilities and cognitive functions.

The research team treated two groups of rats with the synthetic molecules one hour after the stroke period ended. One group got a sodium salt form of the treatment, the second a methyl-ester form. A third control group received saline.
The rats who received the neuroprotector treatment displayed significantly less damage than the saline group, ranging from 44 percent to 81 percent fewer lesions in various parts of the brain. They also demonstrated lower water volume, a sign of less damage following ischemic stroke. In both measures, the methyl-ether results outpaced sodium salt results.

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