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.

Thursday, December 28, 2017

Demystifying chronic fatigue syndrome

We should be able to take this and use it to jumpstart an understanding of post stroke fatigue. Do we have any stroke researcher in the world willing to spend years tackling and solving this problem for the millions of stroke survivors that have this every year? An easy foundation grant to write for our fucking failures of stroke associations. But nothing will occur since we have NO stroke leadership.

Demystifying chronic fatigue syndrome

For years, infectious disease expert Jose Montoya, MD, has been frustrated by the mysteries of chronic fatigue syndrome (also known as myalgic encephalomyelitis) and the unexplainable and often debilitating symptoms of the many patients who come through his clinic at Stanford. But earlier this year, Montoya’s perseverance was rewarded and his optimism soared following a seven-year study he led that showed that the disease has a clear link to 17 immune system proteins, including 13 proteins that are pro-inflammatory.
This proved what scientists had suspected — that inflammation is the prime driver behind the disease, which affects between one and four million people, often with devastating effects. When the finding first came to light, Montoya told me he was “ecstatic.”
“This is telling the world that we have finally a biological correlate for these patients’ symptoms,” he said to me in a recent Q&A for Stanford Medicine News. “These patients are not crazy. Our findings validate their symptoms — that their illness is real and has a biological basis. Now that we know that this is something real, ingrained in the biology of the body and the immune system that explains why these patients are so sick, we could end up with a blood test, but equally or more exciting, now we can find drugs to conquer the disease.”
In the study, the researchers analyzed blood samples from 200 patients, comparing them to 400 controls. Among the CFS patients, they found 17 immune system molecules known as cytokines that tracked the patients’ symptoms and the severity of their illness. Some of these cytokines were associated with inflammation. In recent years, scientists have developed the ability to measure this kind of inflammation, meaning it may be possible to produce a blood test for the disease, Montoya said.
Even more important, he said, is that these patients might ultimately be offered some form of treatment for the illness, which currently isn’t available. Montoya noted that other inflammatory conditions, such as lupus and rheumatoid arthritis, are treatable, so there’s no reason to believe CFS is any different.
“Now that the study has established that it’s inflammatory, we can look for those drugs that treat inflammation,” Montoya said. “I could die happy if I knew that was the door that was opened.”
Montoya collaborated in the study with Mark Davis, MD, PhD, director of Stanford’s Institute for Immunity, Transplantation and Infection.
Previously: Blood test: Scientists crack code of chronic fatigue syndrome’s inflammatory underpinningsStanford researcher develops tools to understand chronic fatigue syndromeA look at the fight against chronic fatigue syndrome and Unbroken: A chronic fatigue syndrome patient’s long road to recovery
Photo by Steve Fisch

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