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.

Showing posts with label Joyce Hoffman. Show all posts
Showing posts with label Joyce Hoffman. Show all posts

Saturday, December 19, 2020

Strokes take years off life, and life out of years

I've been using this 5 year one; you lost 5 cognitive years from the stroke.

Joyce Hoffman mentions losing 9 years in this post:

Oxygen Getting to Brain Cells Is the Problem During Stroke, But Wait! There's Possible Relief Heading Your Way!

You'll have to ask your doctor EXACTLY what protocols they have for you to not lose any years.

 

Strokes take years off life, and life out of years

Having a stroke could not only rob you of years of life; it takes a heavy toll on quality of life as well, a new study finds. Managing hypertension is one key way to avoid stroke.
(Andrew Harrer)

Having a stroke, or even a transient ischemic attack (a TIA, often called a “mini-stroke”) can be a costly watershed in a person’s life. Statistically, it deducts years from patients’ lives. But it claims another toll too: in quality of life after the stroke has happened. New research tallies the combined cost of those two very different measures, and suggests that current treatments for stroke aren’t doing nearly enough to minimize strokes’ true cost.

The study, published Wednesday in the journal Neurology, is an exercise in health economics that seeks to generate a fuller picture of a disease’s cost. That calculation gives insurers, hospital administrators and public health officials a better -- and hopefully more humane -- basis for deciding which treatments are most “cost-effective.”

If a treatment for stroke -- the costly administration of the clot buster called tissue plasminogen activator, or tPA, for instance -- saves people from dying when properly used (as it does), that’s a plus. But if it also reduces disability and allows more stroke patients to return to fuller function than they would have without it, that’s even better. The treatment has not only added years to life, it has added life to years, and that makes it a better treatment.

So what, on the other side of the ledger, does stroke cost? The authors of the latest research followed for five years 440 patients who had arrived at a hospital in Britain suffering from a first TIA and 748 patients who were diagnosed as having had a full-on stroke for the first time.

They found that in the five years after the event, patients who suffered their first stroke lost, on average, 1.71 years due to early death and 1.08 years due to reduced quality of life. If the stroke had never happened, the patient would have had, in principle, five good years; the stroke, by this measure, robbed him or her of 2.79 years, leaving 2.21 good years.

The severity of the stroke obviously resulted in differences within this broad group. Patients judged to have had a mild stroke lost 2.16 quality-years; those who suffered a moderate stroke lost 3.35 good years; severe stroke victims forfeited 4.3 good years.

Patients who suffered their first transient ischemic attack fared better, on average: They lost an average of 0.71 of the next five years to early death, the researchers found. But the patients assessed that over the five years following their TIA, their lost quality of life equaled almost a full good year (or, 0.97 years, to be exact). The result was that their TIA left them 3.32 of the five good years they might otherwise have expected.

The conclusion: There’s a whole lot more that could be done to reduce strokes’ toll. Prevention may be the best strategy -- improving Americans’ control of hypertension, better managing diabetes, bringing more patients with atrial fibrillation and sleep apnea into treatment all would help. But better clot-busting medications and devices, and more widespread use of them, would also help.

Finally, in stroke, physicians emphasize that “time is brain”: the quicker you recognize the signs of an incipient stroke, and the faster you get to a hospital, the more you stand to claim of the five good years ahead. Don’t drive to the hospital or let someone else take you. Call 911.

 

Thursday, August 3, 2017

The 10 best stroke blogs

Well, I didn't make it. The worthless WSO one did, Joyce Hoffman, Rebecca Dutton and Peter Levine are in the top 10.  I bet I have more page views than all of these 10 combined.Oh well, I'll continue shouting into the void.  Friends could comment to
http://www.medicalnewstoday.com/articles/318800.php

Monday, May 16, 2016

What counts as ‘medical marijuana’ varies from state to state – and that’s a problem

Don't worry, none of this applies to stroke patients. None of the state laws I've read have any reference to stroke uses. There is some research out there.
My 13 reasons for marijuana use post-stroke. Don't follow me but I will figure out some way to get some after my next stroke.
Joyce Hoffman lays out the state by state prohibitions and penalties for marijuana possession.
In fact it is fucking stupid for legislators to be proposing medical rules. They should lay out what clinical research is needed to prove efficacy for any disease use for any prohibited drug. Then as clinical trials conclude new diseases are automatically included. 

https://theconversation.com/what-counts-as-medical-marijuana-varies-from-state-to-state-and-thats-a-problem-57084

Tuesday, August 26, 2014

Overweight causes hazardous inflammations

More empirical data about why you need to lose weight. Joyce Hoffman writes about that here also.

This kind of leads to wondering if the mini fasts that slow down Alzheimers would be connected to this response.

To Stave off Alzheimer’s, Stay Hungry?

Researchers: Mini-Fast Prevents Alzheimer's

But don't do these mini-fasts without your doctors prescription, damned dangerous they are.

Overweight causes hazardous inflammations


Researchers have found a possible molecular explanation for why overweight is harmful. This new knowledge may provide new drugs for heart attack, stroke, cancer and chronic intestinal inflammation.
We believe that there is a connection between metabolism, inflammation, heart attack and stroke,” says Bente Halvorsen, professor at the Research Institute for Internal Medicine, University of Oslo, Norway. Together with the research group’s leader, Pål Aukrust, who last year received the university’s research award for his work on inflammatory diseases, and researcher Arne Yndestad, she has looked deeply into the molecular explanation of why overweight is harmful. “With this new knowledge, we can better understand why too much food can cause such serious diseases as heart attack, stroke, cancer and chronic intestinal inflammation.”
We eat too much
Malnutrition and insufficient nutrition lower the immune response, and this increases the risk of infections. If the immune defence system functioned normally, the body would respond with an inflammation to rid itself of the infection. When the immune defence system is impaired, the body is unable to defend itself through inflammation.
Overeating increases the immune response. This increased immune response causes the body to generate excessive inflammation, which may lead to a number of chronic diseases.
“It is therefore important to keep a balance. Too little and too much nutrition may both upset the immune defence system and increase the risk of disease.”
A number of diseases are caused by inflammation. Arthritis is a chronic inflammatory disease. Heart attack is an example of a disease that causes an acute and powerful inflammatory reaction.
“We can reduce the inflammatory reaction by losing weight. Some people risk never getting rid of the inflammation. We have attempted to understand what is needed to reduce the inflammatory reaction without having to lose weight,” Halvorsen explains.
Unfortunately, storage of energy causes an inflammatory reaction. The explanation lies in the close connection between the body’s immune system, energy conversion and the way in which we store energy. It can all be explained in terms of evolution. In our ancestors many hundred million years ago, this was all concentrated in one single organ, like in the modern-day fruit fly. Even though in humans this task is divided among three organs – the fatty tissue that stores energy, the liver that converts energy and the immune system – these organs still communicate closely with each other.
Evolutionarily speaking, humans are not made to eat so much on the contrary; they are intended to toil for their food.
“Mankind’s great challenge has consisted in obtaining sufficient food and surviving infections. Today, we rarely die of infections, but on the other hand we eat too much,” says Arne Yndestad.
Damage to the powerhouse in the cells
The researchers believe that overeating may cause stress to the mitochondria. The mitochondria are the cells’ powerhouses, converting fatty acids to energy.
Evolutionary biologists believe that mitochondria were bacteria that as life has developed have become an integrated part of our cells. The immune system may nevertheless perceive the mitochondria as foreign bodies. Much immunological research therefore focuses on the mitochondria.
When fatty acids accumulate in the cells, the mitochondria become stressed and gradually also damaged.
“When the cells receive excessive energy, the system starts to falter, and the engine may stall. Too much fatty acid causes an oxidative stress in the cells. We believe that long-term stress on the mitochondria may cause metaflammation. A metaflammation is a low-grade chronic inflammation over many years, and unfortunately it’s a condition that’s difficult to detect,” says Yndestad.
The body has its own defence system, called autophagy, which should eliminate damaged mitochondria. When we overeat, free fatty acids accumulate in the cells. This stresses the mitochondria. The stress in the cells causes damage to the mechanism that should eliminate the mitochondria.
When damaged mitochondria accumulate, the immune response is activated. This immune response is exactly what causes the inflammation.
Key signal molecules have been found
The UiO researchers, who also work at the new K.G. Jebsen Inflammation Research Centre, have studied some of the signal molecules inside the cells that trigger the inflammatory reaction. In other words, they have found one element of the energy conversion that may explain what happens when the mitochondria are dealing with the fatty acids. The special element, which is also an enzyme, has previously been studied in stroke patients.
“We believe that this enzyme can be regulated by overnutrition and that it is a key constituent in the inflammatory reaction. We have found that the plaque in the arteries of patients with arteriosclerosis contained a lot of this enzyme. When the plaque bursts, the patient may suffer a stroke,” Halvorsen points out.
In trials with mice, the researchers have tested what happens when the amount of this special enzyme is increased. It reduced the degree of arteriosclerosis.
Strengthening the theory
Their theory was strengthened when they studied how the absence of inflammasomes had an effect on heart function. Inflammasomes are part of the intra-cellular immune defence system.
“When the cells received excessive amounts of fatty acids, the inflammasomes were activated, causing an inflammation.”
Mice with heart attacks functioned better when the inflammasomes were removed.
“So this is about restoring the balance in the immune defence system”, says Yndestad .
A correlation with cancer
The researchers believe that their new discovery may also be a key mechanism in the development of cancer.
“Cancer cells need access to a lot of energy to divide. The cellular stress may transform cells to cancer. Studies of overweight may therefore give us a better understanding of cancer,” Halvorsen explains.
One who is particularly interested in this research is Professor Kristin Austlid Taskén at the Institute for Cancer Research.
“People who are overweight more often develop an aggressive variant of prostate cancer. Although the connection between overweight and cancer is well known, however, little is known about the mechanisms involved” Taskén says.
Her specialty is prostate cancer, a disease that strikes 5000 Norwegians each year.
“Since this is the most common form of cancer among men, it is essential to obtain more knowledge about the way in which overweight affects the metabolism of the cancer cells and leads to aggressive prostate cancer. For the cancer cells to be able to divide rapidly, they make use of new metabolic pathways that are quite unknown to us today. It is therefore useful to have more knowledge that can help us find new drugs that can dispose of the cancer cells,” Taskén points out to the research magazine Apollon.
http://www.apollon.uio.no/english/articles/2014/3_inflammations.h

Wednesday, May 28, 2014