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:http://oc1dean.blogspot.com/2010/11/my-background-story_8.html

Monday, September 25, 2017

New app picks up signs of stroke risk through your smart device

I wouldn't want this, it seems like it would drain my battery and I wouldn't want video being taken without my control. I never take selfies and I highly doubt most elderly people do. And then I would have to switch the camera from front to back. when I want to use it.
http://www.democratandchronicle.com/story/news/2017/09/18/looking-early-signs-heart-trouble-new-app-help/678184001/
You do a lot of things on your phone and tablet.
Now, they may be able to something for you — predict your risk of stroke or heart failure.
Scientists at the University of Rochester Medical Center and the Rochester Institute of Technology teamed up to use the camera on your smart device to pick up changes in your skin color that are too subtle for the eye to see.
“I call it a useful selfie,” said Jean-Phillippe Couderc, associate professor of cardiology at URMC, who helped develop and now is testing an app to detect the irregular heartbeat of atrial fibrillation, AF. “Everybody takes a selfie and shows their face. … This is a new way of using this kind of behavior.”
The app has been tested in the hospital with people who’ve undergone treatment for AF. The next step is to test it at home with people who have experienced AF to see if the app is as sensitive in a less controlled setting.
The research team received a $2 million grant from the National Institutes of Health. By spring, the team will begin to enroll up to 300 people who have been treated for AF to test the app outside a hospital setting.
Couderc and Gill Tsouri, associate professor in the department of electrical & microelectronic engineering at RIT, explain:
What does the app do?
The app runs in the background while the person uses the device to do the usual activities — watch a movie, read, scroll Facebook or do email. Every so often, the app takes a 15- to 20-second video. Using sophisticated algorithms, those images can show changes in the face caused by the heart pumping blood. Based on what it sees, the app can infer cardiac activity.
Why is this big deal?
AF happens when the heart’s two upper chambers beat out of rhythm. AF can lead to serious problems — risk of stroke is five times higher in people with AF, according to the American Heart Association.
Treatments are available, but many people don’t have symptoms such as dizziness, palpitations or shortness of breath, and so they don’t think they are at risk.
Aren’t there other ways to detect AF?
You can have an exam by your doctor, or use sensors that attach to your finger or earlobe. But those require you to do something. With this app, you wouldn’t have to do anything special. People spend a lot of time with smart technology, and this wouldn’t intrude on their day.
Sounds like Big Brother is watching. What happens with the video?
The images are not stored. Once the information is extracted, the videos are deleted.
Who came up with the idea?
Scientists from RIT and URMC regularly get together to exchange ideas, and this one hatched at such a meeting. It has taken about five years to get to this point.
Who is eligible for the study?
Right now, only people who have AF and are treated at URMC will be considered. The researchers want to make sure the app will pick up the signs in people who are known to have the condition, and this way they are able to save money by not having to screen the general population.

NHS 'sleepwalking into stroke crisis' unless more funding found for research into prevention

This is the wrong goal. The goal should be to save as many neurons as possible. That could be prevention or it could be stopping the neuronal cascade of death by these 5 causes in the first week.
http://www.heraldscotland.com/news/15542549.NHS___39_sleepwalking_into_stroke_crisis__39__unless_more_funding_found_for_prevention/
THOUSANDS of people in Scotland could be saved from having a stroke by 2035 if research into the latest stroke prevention procedures were properly funded, according to a report published today.
Stroke is the third most common killer in Scotland and the leading cause of disability, but most strokes can be avoided.
A report, by the Stroke Association and carried out at Queen Mary University of London and London School of Economics, estimates that a £10 million investment in research into interventions such as blood pressure management, treatments for atrial fibrillation which increases the risk of stroke, and treatments to prevent haemorrhagic stroke - the deadliest type - would cut by 114,000 the number of people living with a stroke in UK by 2035.
The report also called for additional research cash for physical and cognitive rehabilitation, vascular dementia and thrombectomy - the emergency surgical removal of blood clots.
The report projects that the annual cost to the NHS of stroke are set to treble from £3.4 billion in 2015 to £10.2 billion in 2035, but that targeted spending in these priority research areas in the next few years "could generate benefits that substantially reduce the burden of stroke by 2035".
The report also estimates that the number of first-time strokes among people over 45 will increase 59 per cent by 2035, but that there will be a 123 per cent increase in the number of patients surviving.
Andrea Cail, Director Scotland of the Stroke Association, said: “The annual number of stroke survivors is expected to increase dramatically by 2035. It’s clear that we need to act now to prevent the UK from sleepwalking towards a stroke crisis.”
Around 145,000 people in Scotland are known to suffer from atrial fibrillation (AF) - a heart condition that causes an irregular and often abnormally fast heart rate. The condition increases the risk of stroke five-fold.
However, many patients are on a treatment that is not effectively lowering their stroke risk, while an estimated 49,414 people in Scotland are living with undiagnosed AF.
High blood pressure, the biggest controllable risk factor for stroke, can also go undetected or poorly managed.
Ms Cail added: “Stroke causes a greater range of disabilities than any other condition, but research into stroke remains underfunded. For example, haemorrhagic stroke is the most deadly type of stroke, and those patients who do survive are more likely to experience severe disability. Currently there are no effective treatments for these strokes, which are caused by bleeds rather than clots in the brain.
"We urgently need to find effective ways to prevent the devastation that haemorrhagic stroke can bring, as well preventing and managing conditions that increase the risk of stroke, such as AF and high blood pressure.”
Across the UK, the annual medical research-spend per stroke patient is £48, compared with £241 per cancer patient and £118 per dementia patient.
Professor Anita Patel, who led the research, said: “Increasing our investment into stroke research will help us turn the tide for people with a higher risk of stroke, allowing us to take steps to prevent the condition more widely. For example, we know that current treatments for high blood pressure do not work for everyone, and are not always used properly.
"More research could help us discover which medication and dosage works best for different people, ensuring we can help prevent more people from having a stroke. This in turn would help to ease the pressure on the already overstretched NHS budgets.”
CASE STUDY:
CHARLIE Ross first knew something was wrong when he got up for work one Friday morning in May 2010 and could not move his leg high enough to climb into the shower cubicle.
"I just said to my wife 'I think you need to take me to hospital - there's something bad here'," he said.
Mr Ross, from Bishopton in Renfrewshire, was only 54 at the time and was shocked when doctors diagnosed a "mini-stroke", or TIA (transient ischaemic attack). It is caused by a temporary disruption of blood flow to the brain and is a warning sign that the patient is at a significantly increased risk of a full stroke in the near future.
Mr Ross was discharged with aspirin and told to rest, but on the Saturday night he suffered a serious attack.
He said: "When I went down to get my dinner I felt kind of woozy. I thought I would just get better, but I couldn't eat my dinner and when I got up from the dining room I got about 20ft and just lost everything on the right-hand side of my body - my leg, my arm, and ended up on the floor in this alcove. That was it - I'd taken another stroke."
Mr Ross, who was then a regional account sales manager, spent three weeks recovering in hospital but seven years on he says his right-arm is "pretty useless" and his walking laboured. He took redundancy in 2014 and helps out in clinical trials into stroke, but says the fatigue following the stroke can be "unbelievable".

Sunday, September 24, 2017

A Drug Might Heal Spinal Injuries By Sparking Nerve Growth

Of course this is in rats and other research possibilities never seem to have made it into clinical practice, so don't get your hopes up on this. Nothing will occur. Nobody will think about possibly using this for stroke survivors because there aren't two functioning neurons in all of stroke medical leadership.
2 posts on chondroitin sulfate proteoglycans back to March 2014.
1 post on heparan sulfate proteoglycans back to March 2014.
1 post on NG2 proteoglycan back to December 2015.
2 earlier posts on proteoglycans back to January 2014.

http://www.npr.org/sections/health-shots/2014/12/03/368058568/a-drug-might-heal-spinal-injuries-by-sparking-nerve-growth
A scientist who chose to ignore the mainstream nearly 30 years ago has found a new way to regenerate nerves in the spinal cord, at least in animals. A drug that Jerry Silver, a professor of neuroscience at Case Western Reserve University, helped design a drug that has allowed paralyzed rats to regain bladder function and even walk.
The drug works by releasing nerve fibers that have become trapped in scar tissue after a spinal cord injury, Silver says. "Now we've got something that might work in people," though it hasn't been tested in humans yet, he says.
The study was published Wednesday in Nature.


The research that led to this drug began in the 1980s. At the time, Silver and many other scientists were studying nerves. "Everybody else in the world was asking why nerves grow where they do," he says. "And I thought I'd do something different and ask why they don't grow where they don't."
Silver figured the body must produce a substance that acts like a sort of guardrail – preventing nerves from going where they are not supposed to. And after about five years of searching, he found a substance in cartilage called a proteoglycan that could redirect a growing nerve. Silver's team published their finding in the early 1990s. "Nobody believed it," he says.
It took another 10 years to convince the scientific world that the finding was real. And even then, the discovery didn't get much attention until Silver realized that the proteoglycan he had discovered played a big role in spinal injuries and paralysis.


Eventually, just a few years ago, Silver and Harvard biologist John Flanagan showed that the proteoglycan interacts with severed nerve fibers in a way that glues the fibers to scar tissue "like a fly on flypaper."
That got Silver thinking about people who are paralyzed because of damage to nerve fibers in the spinal cord. "You've got an untapped source of nerve fibers," he says. "Thousands upon thousands of them, you know, sitting around just waiting to be released."
Silver thought if he could release these trapped fibers, the nerves might be able to regenerate. So his team designed a drug that was able to free nerve fibers in a Petri dish. Then they tried the drug on rats with spinal injuries that left them unable to walk and without bladder control.
A graduate student gave the animals daily injections under the skin, Silver says. But after seven weeks of treatment, the rats weren't any better and the student asked if he could stop giving the injections. "I said fine, we'll quit," Silver says. "We put the rats aside and about two to three weeks later they started to improve."
The injections really had freed the trapped nerve fibers and they had begun growing. But that didn't fix the problem the way you might think. The severed nerve ends were not reconnecting. Instead they were sprouting all over the place, like kudzu. And all this new growth was flooding the spinal cord with the hormone serotonin.
It was this new supply of serotonin that was helping the rats function by amplifying the signals carried by nerves that were still intact. "If you have lots of extra serotonin in the spinal cord those few nerve connections that are just a whisper will become a roar," Silver says. "And you can get function back really nicely."
All of the paralyzed rats that got a high dose of the drug regained some bladder control and a third were able to walk again, Silver says.
The new drug represents an important step forward, says Lyn Jakeman, a program director at the National Institute of Neurological Disorders and Stroke, which helps fund Silver's research. One reason, she says, is that it can be injected under the skin.
Other promising treatments, such as stem cells, risk causing more damage because they can disturb the part of the spinal cord that is already injured, Jakeman says. "They're all very invasive."
The new drug also was remarkably effective at improving bladder function, Jakeman says, which is a major concern for many paralyzed people. "A small change in bladder function, the ability to restore a small amount of sexual function, these are big changes for people whether they can get out of their wheelchair and walk or not."

Mediterranean style diet may prevent dementia - 34-53% lower chance

Well, ask your doctor for a definitive diet protocol. SPECIFICS, NOT generic crap like the MIND or Mediterranean diets. I expect specific amounts per body weight and sex on a daily basis. How much olive oil should you be consuming? How much red wine should you be consuming? Anything less than that is incompetence.  
http://www.cnn.com/2017/07/17/health/mediterranean-style-diet-prevents-dementia/index.html
(CNN)Meals from the sunny Mediterranean have been linked to stronger bones, a healthier heart and longer life, along with a reduced risk for diabetes and high blood pressure.
Now you can add lowering your risk for dementia to the ever growing list of reasons to follow the Mediterranean diet or one of its dietary cousins.
New research being presented at the Alzheimer's Association International conference in London this week found healthy older adults who followed the Mediterranean or the similar MIND diet lowered their risk of dementia by a third.
"Eating a healthy plant-based diet is associated with better cognitive function and around 30% to 35% lower risk of cognitive impairment during aging," said lead author Claire McEvoy, of the University of California, San Francisco's School of Medicine.
McEvoy stressed that because the study was conducted in a nationally representative older population "the findings are relevant to the general public."
"While 35% is a greater than expected decrease for a lifestyle choice, I am not surprised," said Rudolph Tanzi, who directs the Genetics and Aging Research Unit at Massachusetts General Hospital and recently co-authored a book with Deepak Chopra on genes and aging called "Super Genes."
"The activity of our genes is highly dependent on four main factors: diet, exercise, sleep and stress management," said Tanzi, who was not involved in the study. "Of these, perhaps diet is most important."
McEvoy's study investigated at the eating habits of nearly 6,000 older Americans with an average age of 68. After adjusting for age, gender, race, low educational attainment and lifestyle and health issues -- such as obesity, hypertension, diabetes, depression, smoking and physical inactivity -- researchers found that those who followed the MIND or Mediterranean diet had a 30% to 35% lower risk of cognitive impairment.
The more people stayed on those diets, said McEvoy, the better they functioned cognitively.
Those who marginally followed the diet also benefited, but by a much smaller margin. They were 18% less likely to exhibit signs of cognitive impairment.

What are the Mediterranean and MIND diets?

Forget lasagne, pizza, spanakopita and lamb souvlaki -- they are not on the daily menu of those who live by the sunny Mediterranean seaside.
The true diet is simple, plant-based cooking, with the majority of each meal focused on fruits and vegetables, whole grains, beans and seeds, with a few nuts and a heavy emphasis on extra virgin olive oil. Say goodbye to refined sugar or flour and fats other than olive oil, such as butter, are consumed rarely, if at all.
Meat can make a rare appearance, but usually only to flavor a dish. Instead, meals may include eggs, dairy and poultry, but in much smaller portions than in the traditional Western diet. Fish, however, are a staple.
The MIND diet takes the best brain foods of the Mediterranean diet and the famous salt-reducing DASH diet, and puts them together. MIND encourages a focus on eating from 10 healthy food groups while rejecting foods from five unhealthy groups.
MIND stands for Mediterranean-DASH Intervention for Neurodegenerative Delay, with DASH standing for Dietary Approaches to Stop Hypertension.
MIND was developed by Martha Clare Morris, a nutritional epidemiologist at Chicago's Rush University Medical Center in the US.
Those who follow MIND reject butter and stick margarine, red meats, cheeses, fried or fast food and sweets. Instead, they eat at least six servings a week of green leafy vegetables such as spinach or kale, and at least one serving a day of another vegetable. Three servings a day of whole grains are a must.
They also add in at least three servings of beans, two or more servings of berries, two servings of chicken or turkey, and once serving of fish each week. Olive oil is their main cooking ingredient, and they drink a glass of wine a day.
Morris has some powerful stats behind her diet.
In 2015, she studied 923 Chicago-area seniors and found those who say they followed the diet religiously had a 53% lower chance of getting Alzheimer's, while those who followed it moderately lowered their risk by about 35%. Follow-up observational studies showed similar benefits.
Morris and her colleagues are currently recruiting volunteers for a three-year clinical study to try to prove the link.

Additional evidence

A second study presented at the conference also examined the impact of the MIND diet. Researchers from Wake Forest School of Medicine followed 7,057 women, average age 71, over almost 10 years and found those who most closely followed the MIND diet had a 34% reduction in the risk of developing Alzheimer's.
A third study at the conference looked at the dietary habits of 2,223 dementia-free Swedish adults over six years who followed the Nordic Prudent Dietary Pattern (NPDP) diet, which avoids sweets and fatty and processed foods. Instead, the diet emphasizes eating non-root vegetables, apple/pears/peaches, pasta/rice, poultry, fish, vegetable oils, tea and water, and light to moderate wine intake.
Swedes who stuck to the diet at a moderate or higher level preserved their cognitive function better than those who ate more processed and fatty foods.
Lastly, a fourth study examined MRI brain scans of 330 cognitively normal adults, with an average age of 79, and found eating foods that raise inflammation in the body -- such as sweets, processed foods and fried and fatty foods -- raised the risk for a shrinking "aging" brain and lower cognitive function.
That comes as no surprise to neurologist Rudy Tanzi.
"Foods that keep blood pressure normal, provide us with antioxidants, and maintain healthy bacteria in our gut, or microbiome, will serve to help keep chronic inflammation in check in the brain and entire body," said Tanzi.
Despite the similarities of the results, experts point out that all of this research is observational, meaning that it is based on reports by individuals as to what they eat. To prove the connection between diet and dementia risk, said McEvoy, researchers will need to move to scientifically controlled experiments.
"I think the studies, taken together, suggest a role for high quality dietary patterns in brain health and for protection against cognitive decline during aging," said McEvoy. "Diet is modifiable, and in light of these studies we need clinical trials to test whether changing diet can improve or maintain cognition."
Join the conversation
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Until that definite proof is available, say experts, there's no harm in using this information to makes changes in your diet and lifestyle that could help protect your brain.
"Although the idea that a healthy diet can help protect against cognitive decline as we age is not new, the size and length of these four studies demonstrate how powerful good dietary practices may be in maintaining brain health and function," said Keith Fargo, Alzheimer's Association Director of Scientific Programs and Outreach.
Tanzi agrees. "It's about time we started placing a greater emphasis on what we eat as we strive to have our 'healthspan' keep up with our increasing 'lifespan'."

Clinical Outcome Measures for Lateropulsion Poststroke: An Updated Systematic Review

Proving once again the incompetence out there in stroke that a review needs to be done at all. There should be a publicly available database of stroke research and protocols updated each time something new comes in. These reviews and meta-analysis are fucking wastes of time getting in the way of actually solving all the problems in stroke.
http://journals.lww.com/jnpt/Abstract/2017/07000/Clinical_Outcome_Measures_for_Lateropulsion.2.aspx

Koter, Ryan PT, DPT; Regan, Sara PT, DPT; Clark, Caitlin PT, DPT; Huang, Vicki DPT; Mosley, Melissa PT, DPT; Wyant, Erin PT, DPT; Cook, Chad PT, PhD, MBA, FAAOMPT; Hoder, Jeffrey PT, DPT, NCS
Journal of Neurologic Physical Therapy: July 2017 - Volume 41 - Issue 3 - p 145–155
doi: 10.1097/NPT.0000000000000194
Systematic Reviews
Watch Video Abstract
Background and Purpose: Contraversive Lateropulsion, also referred to as contraversive pushing, pusher behavior, and pusher syndrome, can be associated with increased hospital length of stay, increased health care costs, and delayed outcomes in persons with stroke. The purpose of this updated systematic review was to identify scales used to classify contraversive lateropulsion, investigate literature that addresses their clinimetric properties, and create a resource for clinicians recommending use in clinical practice.
Methods: Three databases were searched for articles from inception to March 2017. The search strategy followed Cochrane Collaboration guidelines. The Consensus-based Standards for the selection of health Measurement INstruments (COSMIN) checklist was applied to evaluate methodological quality.
Results: Four hundred three records were screened. Seven studies met inclusion criteria. Four scales were identified: the Scale for Contraversive Pushing (SCP), the Modified Scale for Contraversive Pushing (M-SCP), the Burke Lateropulsion Scale (BLS), and the Swedish Scale for Contraversive Pushing (S-SCP). Psychometric property investigation was most robust for the SCP and the BLS. Cross-cultural validity has not been fully investigated in scales used outside of their country of origin.
Discussion and Conclusions: The BLS is recommended for identifying contraversive lateropulsion. The scale assesses the presence of contraversive lateropulsion across several functional tasks, from rolling to walking, and is the only scale originally written in English. The BLS is the only tool to receive ratings greater than poor for reliability and responsiveness. The BLS should be implemented as soon as contraversive lateropulsion is suspected to guide frontline clinicians' initial plan of care, allow objective identification of change over time, and facilitate easier investigation of interventional efficacy.
Video Abstract available for additional insights from the authors (see Video, Supplemental Digital Content 1, http://links.lww.com/JNPT/A177).
© 2017 Academy of Neurologic Physical Therapy, APTA

Dendritic spines provide cognitive resilience against Alzheimer's disease

You'll have to DEMAND your doctor provide you protocols that will create new dendritic spines.  And after s/he does that ask for proof that the protocols are working. You have to DEMAND accountability and responsibility from your doctors.
http://onlinelibrary.wiley.com/doi/10.1002/ana.25049/full

Authors


Abstract

Objective: Neuroimaging and other biomarker assays suggest that the pathological processes of Alzheimer's disease (AD) initiate years prior to clinical dementia onset. However some 30%-50% of older individuals that harbor AD pathology do not become symptomatic in their lifetime. It is hypothesized that such individuals exhibit cognitive resilience that protects against AD dementia. We hypothesized that in cases with AD pathology structural changes in dendritic spines would distinguish individuals that had or did not have clinical dementia.
Methods: We compared dendritic spines within layers II and III pyramidal neuron dendrites in Brodmann Area 46 dorsolateral prefrontal cortex using the Golgi-Cox technique in 12 age-matched pathology-free controls, 8 controls with AD pathology (CAD), and 21 AD cases. We used highly optimized methods to trace impregnated dendrites from brightfield microscopy images which enabled accurate three-dimensional digital reconstruction of dendritic structure for morphologic analyses.
Results: Spine density was similar among control and CAD cases but reduced significantly in AD. Thin and mushroom spines were reduced significantly in AD compared to CAD brains, whereas stubby spine density was decreased significantly in CAD and AD compared to controls. Increased spine extent distinguished CAD cases from controls and AD. Linear regression analysis of all cases indicated that spine density was not associated with neuritic plaque score but did display negative correlation with Braak staging.
Interpretation: These observations provide cellular evidence to support the hypothesis that dendritic spine plasticity is a mechanism of cognitive resilience that protects older individuals with AD pathology from developing dementia. This article is protected by copyright. All rights reserved.

Saturday, September 23, 2017

Don’t overthink your exercise: just 2.5 hours per week of any kind could help you live longer

Sometimes I get that in a day depending upon how slow I'm walking and how hot it is.
https://www.vox.com/science-and-health/2017/9/22/16343458/exercise-2-hours-per-week-live-longer
With the explosion of boutique gyms and spin classes and ultramarathons, it can feel like exercise should be both expensive and extreme. But researchers are finding that it really doesn’t seem to matter what kind of physical activity you do to reap great health rewards.
In one of largest global studies ever published on the heart health benefits of physical activity, researchers found that 150 minutes spent exercising per week could cut a person’s risk of cardiovascular disease and death. And, most importantly, the Lancet paper demonstrated that all kinds of physical activity were equally good for the heart.
“I would dispel the notion of having to put out money to be active,” said Dr. Scott Lear, the study lead author and a professor at Simon Fraser University’s Faculty of Health Sciences in Canada, in an email. “Our findings indicate that nonrecreational activity — work, housework, active transportation — is just as beneficial in reducing the risk for premature death and heart disease.”
So, yes, even vacuuming your house or walking on your lunch hour for a solid 30 minutes can help avert an early death and chronic disease.
The researchers tracked the exercise levels — as well as the rate of cardiovascular disease (including heart attacks, stroke, and heart failure) and all-cause mortality — of more than 130,000 adults living in 17 high-, low-, and middle-income countries, from Canada to China.
Following the study participants for an average of seven years, they found the people who reported at least 150 minutes of physical activity per week were much healthier than their sedentary counterparts: They were less likely to have heart attacks, strokes and cardiovascular disease, and less likely to die from any cause. Getting only two and a half hours of weekly exercise was associated with a 28 percent reduction in premature death, and a 20 percent reduction in heart disease.
All forms of exercise appeared to reduce a person’s risk of death and disease, whether people were sweating away in a gym class, cleaning their house, or simply walking to work.
“This is a large study, covering a lot of different countries of different income levels and means of physical activity,” said Brian Elbel, director of NYU’s Langone Comprehensive Program on Obesity, “and it confirms that physical activity is great and focusing on the means of physical activity isn’t important.”

We spend more time glued to our seats, while rates of chronic disease are going up

But while the evidence keeps piling up to show us that physical activity is really important for not dying early, we’re also more sedentary than ever before. Most of us barely manage to meet the minimum exercise requirements — or to carry on the most basic health habits. Only about 38 percent of Americans surveyed in this 2016 Mayo Clinic Proceedings study had a healthy diet, just 10 percent had a normal body fat level — and fewer than half (47 percent) were sufficiently active.
We’re driving more, spending more time in front of screens, and walking less. According to one study of health impact of sedentary behavior, in 1970, only 20 percent of Americans had jobs that required little physical activity (and lots of sitting around). By 2000, that number climbed to 40 percent. All told, Americans now spend up to nine hours each day being sedentary.
Meanwhile, lifestyle-related chronic diseases have shot up dramatically. Having a high body weight contributed to 4 million deaths globally — or 7 percent of the deaths from any cause — in 2015, according to a recent New England Journal of Medicine paper. Most of those deaths were caused by cardiovascular disease, with diabetes following closely behind, along with kidney disease and cancers.

The easiest ways to exercise more without extra time

Americans often complain that they don’t have enough time to work out. A 2015 survey asked a group of 1,000 of them how they'd spend an extra four hours each week if they suddenly had the time. The number one answer? Exercise. The desire for more time to work out trumped the wish for more time spent with family, sleeping, or even doing hobbies.
But this Lancet paper is a reminder that we often overthink exercise — and we may not actually need to set aside extra time to work out. Exercise doesn't require a gym membership or fancy shoes. Exercise is something you can do throughout the day, every day. It also doesn’t need to be grueling, and it doesn’t have to cost anything, to see health benefits.
So how can you incorporate more physical activity in your waking hours? Simply walking more — while commuting, running errands, or on the phone — counts for a lot, health-wise. Dr. Mike Evans, an associate professor of family medicine and public health at the University of Toronto, has a great video on how to fill your day with more activity. He suggests:
  • Scheduling walking meetings
  • Getting off a stop early on your daily commute to work
  • Walking on your lunch hour instead of going to another place to sit
  • Walking to the grocery store instead of driving
  • If you do drive, park far away
  • Taking the stairs to your office instead of the elevator
The researchers in the Lancet study also found there was a linear relationship between the amount of exercise and disease risk, meaning the more hours a person spent doing physical activity (again, of any kind), the lower their risk of disease and death. (The benefits seemed to taper off at 1.8 hours of brisk walking per day.) And the people who reported getting the most physical activity were the ones who had exercise built into their daily lives, Lear noted, through simple things like active transport to work, their jobs, or doing housework.
“I would also stress that physical activity is a good stress release,” Lear said. “I commute by bicycle to work and that ride home is so good for burning off the stress of the work day and I get home much fresher than if I sat in a car fighting traffic.”

Our physical environment encourages sedentary lifestyles — and that needs to change

As we learn more about the importance of exercise for health, we also have to make our communities more amenable to active lifestyles.
Imagine if more cities made their streets pedestrian-friendly and invested in spaces that everyone could access, such as community yoga studios, public parks, or even programs like Sunday San Francisco Streets or the Ciclovía in Bogota, Colombia, which involve closing down streets for walking and biking on the weekend.
Researchers have also found putting traffic-free cycling and walking routes in place increases physical activity levels for the people who live near them.
These public places offer the most cost-effective forms of exercise, and they’re available to everybody. In this 2011 economic analysis, the researchers found Sunday San Francisco Streets cost only $1.35 per week. Meanwhile, they estimated, using pedestrian trails in Nebraska cost 81 cents, and the weekly cost of private fitness centers in cities like San Francisco runs about $20. Compare that with using a boutique spinning or Pilates studio two or three times per week, for which you can shell out more than $90.
“In high income countries in particular, and in occupations that result in a lot of sitting, we have engineered physical activity out of our daily work or domestic lives,” Lear said. We’ve also made working out too complicated. Science suggests that should change.


Aspirin taken to thin the blood to prevent strokes 'can double risk of suffering a heart attack'

Danger, danger Will Robinson. Ask your doctor what to do.  I've been told I don't have afib, but that was after listening to my heart for 30 seconds.
How do they test for atrial fibrillation?
Your doctor may order several tests to diagnose your condition, including:
  1. Electrocardiogram (ECG). ...
  2. Holter monitor. ...
  3. Event recorder. ...
  4. Echocardiogram. ...
  5. Blood tests. ...
  6. Stress test. ...
  7. Chest X-ray.
http://www.dailymail.co.uk/health/article-4337050/Aspirin-double-risk-suffering-heart-attack.html
  • Study of 30,000 NHS patients with atrial fibrillation found they were at higher risk if they took aspirin
  • Patients were 1.9 times as likely to have an acute heart attack, it found
  • Research carried out by Southampton University and Maastricht University 
Aspirin taken by thousands of people to thin the blood and ward off strokes could double the risk of heart attacks, experts have warned.
A study of 30,000 NHS patients found those with atrial fibrillation - a heart condition that causes an irregular and often abnormally fast heart rate - were at higher risk if they took aspirin than other drugs.
Researchers from Southampton University and Maastricht University in the Netherlands examined health records of people who were prescribed warfarin, aspirin or a new generation of pills to prevent stroke.
They found patients who took aspirin were 1.9 times as likely to suffer an acute heart attack as those who took warfarin, one of a class of drugs called vitamin K antagonists.
A study of 30,000 NHS patients found those with atrial fibrillation - a heart condition that causes an irregular and often abnormally fast heart rate - were at higher risk if they took aspirin than other drugs
Study leader Dr Leo Stolk, from Maastricht, said: ‘Oral anticoagulant treatment with vitamin K antagonists has been the cornerstone for the prevention of stroke in patients with atrial fibrillation for decades.
‘We identified an ... increased risk of [heart attacks] among current and past aspirin users in comparison with VKAs.
‘There also exists doubt about the usefulness of aspirin in atrial fibrillation. In new guidelines aspirin is no longer included.’
The paper, published in the British Journal of Clinical Pharmacology, found a new class of drugs called direct oral anticoagulants - or DOACs - were also linked to a doubling in heart attack risk.
The study looked at prescription history and heart problems among NHS patients - 15,400 who were users of aspirin, 13,098 of VKAs, 1,266 of DOACs or 382 who took a mixture.

The Role of the BDNF Val66Met Polymorphism in Recovery of Aphasia After Stroke

I understood nothing in this, can't even begin to figure out how this is going to help you recover from aphasia.
http://journals.sagepub.com/doi/abs/10.1177/1545968317723752
First Published August 17, 2017 Research Article


Background. Brain-derived neurotrophic factor (BDNF) is assumed to play a role in mediating neuroplasticity after stroke. Carriers of the function-limiting Val66Met (rs6265) single nucleotide polymorphism (SNP) may have a downregulation in BDNF secretion, which may lead to a poorer prognosis after stroke compared to noncarriers in motor learning and motor function recovery. The present study investigates whether this polymorphism may also affect the recovery of poststroke aphasia (ie, language impairment).  
Objective. To study the influence of the BDNF Val66Met polymorphism on the recovery of poststroke aphasia.  
Methods. We included 53 patients with poststroke aphasia, all participating in an inpatient rehabilitation program with speech and language therapy. All patients were genotyped for the Val66Met SNP and subdivided into carriers (at least one Met allele) and noncarriers (no Met allele). Primary outcome measures included the improvement over rehabilitation time on the Amsterdam-Nijmegen Everyday Language Test (ANELT) and the Boston Naming Test (BNT).  
Results. The outcome measures showed a large variability in the improvement scores on both the ANELT and BNT. There was no significant difference between noncarriers and carriers in the primary outcome measures.  
Conclusion. This study investigated the effect of the BDNF Val66Met polymorphism on clinical recovery of poststroke aphasia. In contrast to earlier studies describing a reducing effect of this polymorphism on motor function recovery after stroke, the present study does not support a reduction in language recovery for carriers compared to noncarriers with poststroke aphasia.

Lower Extremity Motor Impairments in Ambulatory Chronic Hemiparetic Stroke: Evidence for Lower Extremity Weakness and Abnormal Muscle and Joint Torque Coupling Patterns

Well fuck, more laziness. Describe a problem but give NO solutions and still followup is required.
http://journals.sagepub.com/doi/abs/10.1177/1545968317721974
First Published August 8, 2017 Research Article


Although global movement abnormalities in the lower extremity poststroke have been studied, the expression of specific motor impairments such as weakness and abnormal muscle and joint torque coupling patterns have received less attention. We characterized changes in strength, muscle coactivation and associated joint torque couples in the paretic and nonparetic extremity of 15 participants with chronic poststroke hemiparesis (age 59.6 ± 15.2 years) compared with 8 age-matched controls. Participants performed isometric maximum torques in hip abduction, adduction, flexion and extension, knee flexion and extension, ankle dorsi- and plantarflexion and submaximal torques in hip extension and ankle plantarflexion. Surface electromyograms (EMGs) of 10 lower extremity muscles were measured. Relative weakness (paretic extremity compared with the nonparetic extremity) was measured in poststroke participants. Differences in EMGs and joint torques associated with maximum voluntary torques were tested using linear mixed effects models. Results indicate significant poststroke torque weakness in all degrees of freedom except hip extension and adduction, adductor coactivation during extensor tasks, in addition to synergistic muscle coactivation patterns. This was more pronounced in the paretic extremity compared with the nonparetic extremity and with controls. Results also indicated significant interjoint torque couples during maximum and submaximal hip extension in both extremities of poststroke participants and in controls only during maximal hip extension. Additionally, significant interjoint torque couples were identified only in the paretic extremity during ankle plantarflexion. A better understanding of these motor impairments is expected to lead to more effective interventions for poststroke gait and posture.

Agreed Definitions and a Shared Vision for New Standards in Stroke Recovery Research: The Stroke Recovery and Rehabilitation Roundtable Taskforce

I still don't see this as helping because they could agree on using the Rankin scale which has zero objectivity. I see the need for objective damage diagnosis like 3d scans of the dead and damaged areas mapped to external disabilities.  Until we get to those two points none of this stroke research is repeatable. You can have 9 different reasons for the same external disability and there is no way one intervention will correct all nine. And since they are hiding the paper behind a paywall, we can't tell how bad it is and get our non-existent stroke leadership to correct it.
1. Penumbra damage to the motor cortex.
2. Dead brain in the motor cortex.
3. Penumbra damage in the pre-motor cortex.
4. Dead brain in the pre-motor cortex.
5. Penumbra damage in the executive control area.
6. Dead brain in the executive control area.
7. Penumbra damage in the white matter underlying any of these three.
8. Dead brain in the white matter underlying any of these three.
9. Spasticity preventing movement from occurring.
http://journals.sagepub.com/doi/abs/10.1177/1545968317732668
First Published September 21, 2017 Research Article


The first Stroke Recovery and Rehabilitation Roundtable established a game changing set of new standards for stroke recovery research. Common language and definitions were required to develop an agreed framework spanning the four working groups: translation of basic science, biomarkers of stroke recovery, measurement in clinical trials and intervention development and reporting. This paper outlines the working definitions established by our group and an agreed vision for accelerating progress in stroke recovery research.

Standardized Measurement of Sensorimotor Recovery in Stroke Trials: Consensus-Based Core Recommendations from the Stroke Recovery and Rehabilitation Roundtable

No use of the word objective so this will be useless. No objective starting point or mention of a damage diagnosis so nothing is repeatable.
http://journals.sagepub.com/doi/abs/10.1177/1545968317732662
First Published September 21, 2017 Research Article


Finding, testing and demonstrating efficacy of new treatments for stroke recovery is a multifaceted challenge. We believe that to advance the field, neurorehabilitation trials need a conceptually rigorous starting framework. An essential first step is to agree on definitions of sensorimotor recovery and on measures consistent with these definitions. Such standardization would allow pooling of participant data across studies and institutions aiding meta-analyses of completed trials, more detailed exploration of recovery profiles of our patients and the generation of new hypotheses. Here, we present the results of a consensus meeting about measurement standards and patient characteristics that we suggest should be collected in all future stroke recovery trials. Recommendations are made considering time post stroke and are aligned with the international classification of functioning and disability. A strong case is made for addition of kinematic and kinetic movement quantification. Further work is being undertaken by our group to form consensus on clinical predictors and pre-stroke clinical data that should be collected, as well as recommendations for additional outcome measurement tools. To improve stroke recovery trials, we urge the research community to consider adopting our recommendations in their trial design.

Friday, September 22, 2017

Placebos are now available on the web from APlacebo.com

Since placebos have been proven to be so effective, get them here yourself. This way you don't have to be in a research project and be in the cohort that gets the placebo rather than the real drug/intervention.
But don't listen to me.
https://www.journalism.co.uk/press-releases/placebos-are-now-available-on-the-web-from-aplacebo-com/s66/a551839/
Chelmsford, England. – 3Bods Ltd make Placebo medicines available to the general public for the first time ever. Never before has the ordinary person been able to go and get Placebos for themselves or their family
Chelmsford, England. – 3Bods Ltd make Placebo medicines available to the general public for the first time ever. Never before has the ordinary person been able to go and get Placebos for themselves or their family. Although used in virtually every drug trial this is the first time that these powerful agents have been available on demand.
Through the website APlacebo.com it is now possible for anyone to purchase Placebo. Prices range from as little as £5.00 for the revolutionary SMS (Text) Placebo upwards. Placebos are available in various formats including solutions, sprays and homeopathic solutions as well as the Placebo to your phone.
As well as having Placebo for sale the website is a mine of information about what Placebos are and how they affect people. There are links to external sites including the NHS, The American Psychological Association and The National Institutes of Health which give full and unbiased information on Placebos and the Placebo effect.  There are also two videos available which explain in simple terms what a Placebo is and the effects they can have.
The Placebo effect is Real and is well documented. Very recently it was reported that at least half of the effectiveness of sleeping pills was due to the Placebo effect (Harvard Medical School and others). Placebos are safe, simple to take and effective. Placebos even work when you know you are taking a Placebo!
About 3Bods – 3Bods is a small firm run by 3 individuals. APlacebo.com is the first commercial website that the firm has created since it was started last year. Its members have all worked in the IT business whilst one of them was working in the NHS for 11 years ending up as a director of Child Health in a large community NHS trust.
Further information – Either via the website or contact 3Bods directly at info@3Bods.co.uk
APlacebo.com – the first website in the world where you can buy Placebos.

Movers & Shakers: Joseph Foecking, director of rehabilitation for UCHealth - Colorado

If you know this guy you need to ask EXACTLY WHAT HE IS DOING TO GET ALL STROKE SURVIVORS 100% RECOVERED, NOT JUST 'CARE'.
http://gazette.com/movers-shakers/article/1611731 
Joseph Foecking, director of rehabilitation for UCHealth Memorial Hospital, has been reappointed by Gov. John Hickenlooper to a three-year term on the Colorado Stroke Advisory Board, which evaluates strategies for stroke prevention and treatment, and develops statewide needs assessments to improve the quality of care for stroke patients. He serves as a representative of a stroke rehabilitation facility.

Researchers discover post stroke neurogenesis in the hippocampus is linked to worse performance in hippocampal memory tasks.

What is your doctor doing to alter this aberrant neurogenesis?
http://neurosciencenews.com/neurogenesis-stroke-hippocampus-7551/

Source: PLOS.
Neurogenesis is a complex biological process by which neurons are generated from neural stem cells and progenitor cells. Indeed, the discovery of a dynamic neurogenesis in the adult brain (in both humans and animals) was a kind of extraordinary revelation. In fact, contrary to common popular belief, neurogenesis continuously occurs in specific regions in the adult brain, such as in the hippocampus and the striatum. Neurogenesis occurs in both physiological and pathological conditions.
In the hippocampus, newly born granule cells (GC) in the subgranular zone of the dentate gyrus (DG) migrate in the granule cell layer and become functionally integrated into neuronal networks within four to six weeks. Interestingly, recent findings suggest that newborn neurons generated in the context of cerebral ischemia may fail to correctly integrate into pre-existing networks. However, the cellular mechanisms of how ischemic infarcts cause alteration of hippocampal functions are only partially understood.

Memory, neurogenesis and morphological alterations following cerebral stroke

In a recent PLOS One article, Woitke and collegues (Jena University Hospital, Germany) hypothesized that increased neurogenesis in the dentate gyrus following stroke may be associated with aberrant neurogenic activity and impaired hippocampus-dependent functions. This might sound somehow counterintuitive, since one would expect that increased neurogenesis may lead to improved cognitive functions. But this is not the case, or at least it does not represent the full and exact picture of what happens.
In fact, it is well known that cerebral stroke stimulates neurogenesis in the adult dentate gyrus, although the functional role of this post-lesion response is mostly unclear. In a physiological context, neurogenesis is strictly regulated and less than 1% of new neurons have aberrant connections in the intact brain. Things may be different following brain damage and insults (strokes, seizures, etc). Using behavioral and viral approaches “we now prove,” says Woitke, the leading author of the study, “that aberrant neurogenesis also occurs in the murine hippocampus and is associated with poorer performance in hippocampal-dependent memory tasks following focal infarcts.”
In a first attempt, Woitke and colleagues performed the Morris Water Maze (MWM), a hippocampus-dependent behavioral task routinely used to assess spatial memory functions. Parameters such as latencies (“time to find the platform”) and distance (“path lengths”) to navigate to the platform were analyzed. As expected, brain ischemic mice generally needed more time to locate the platform, thus suggesting impaired learning and memory functions. In addition, analysis of the adaptive learning strategies in both groups revealed that animals with stroke used a less efficient navigation strategy to find the platform, while hippocampal-dependent strategies were employed more frequently by the control group. When looking at neurogenesis processes the authors observed an increased number of new born neurons in the hippocampus of mice with stroke. Thus, in a second set of experiments, the authors addressed the question of whether the newly generated neurons may have aberrant morphology and location, which in turn may be related to malfunction of hippocampal networks and circuits.
“Using retroviral labeling, we detected a significant number of new GC with atypical morphology and dendritic branching following ischemia,” says Silke Keiner, the senior author of the study. In particular, GC displayed an additional dendritic tree extending from the basal pole towards the hilus (a specific subregion of the dentate gyrus) which is considered a typical immature feature of GC neurons. Taken together, ischemia increases the number of newborn neurons but promotes aberrant dendritic branching indicating maladaptive plasticity in the DG.
Image shows neurons.
In fact, it is well known that cerebral stroke stimulates neurogenesis in the adult dentate gyrus, although the functional role of this post-lesion response is mostly unclear. NeuroscienceNews.com image is credited to the researchers/PLOS ONE
It is worth mentioning that integrated and functional neurons require dendritic spines. Interestingly, the expression of mature mushroom spines by aberrant newborn cells strongly suggests that these neurons are synaptically integrated, thus being able to influence and alter hippocampal networks.

Conclusions

In general, this study reveals that even a low number of aberrant neurons may severely affect hippocampal functions such as learning and memory. However, the casual link among cellular modifications, neurogenesis and impaired memory functions is far from being fully elucidated. In fact, the analysis of the functional impact of adult neurogenesis in behavioral experiments or cognitive tasks is still quite challenging. As mentioned by the authors, “more studies are needed to clarify whether tailored rehabilitative and therapeutic approaches might counteract aberrant neurogenesis and improve hippocampal-dependent memory performance.”
About this neuroscience research article
Source: Giuseppe Gangarossa – PLOS
Image Source: NeuroscienceNews.com image is credited to the researchers/PLOS ONE.
Original Research: Full open access research for “Adult hippocampal neurogenesis poststroke: More new granule cells but aberrant morphology and impaired spatial memory” by Florus Woitke, Mihai Ceanga, Max Rudolph, Fanny Niv, Otto W. Witte, Christoph Redecker, Albrecht Kunze, and Silke Keiner in PLOS ONE. Published online September 14 2017 doi:10.1371/journal.pone.0183463

Can Alzheimer's be stopped years before it starts?

And if we had a great stroke association we could bring together hundreds of institutions together to dole out problems in stroke to solve. But we have fucking failures of stroke associations instead sucking up money that could be put to a better use.  If a vaccine is developed then all stroke survivors should probably get it due to our likely descent into dementia.
https://medicalxpress.com/news/2017-09-alzheimer-years.html?
September 15, 2017 by Erica Rheinschild 
Researchers at the Keck School of Medicine of USC are tackling the sixth-leading cause of death in the United States—Alzheimer's disease—with a new study that intervenes decades before the disease develops.
The school is joining approximately 90 institutions in North America, Europe and Australia in the Generation Study, which is testing a and oral medication to prevent or delay Alzheimer's in older adults at increased risk for developing the disease. More than 70 USC researchers across a range of disciplines are dedicated to the prevention, treatment and potential cure of Alzheimer's.
By focusing on prevention, the study is taking a different approach to halting a disease that affects 47 million people worldwide.
"One of the challenges in developing new medications for Alzheimer's is that researchers tend to test medications on people with more advanced Alzheimer's, and the medications are simply not proving to be effective," Lon Schneider, the study's lead investigator. "By intervening 10 to 12 years before Alzheimer's manifests, we may be able to stop it before it begins or delay the symptoms."
Adults 60 to 75 years of age with normal cognition who are interested in participating must undergo genetic testing for the apolipoprotein e4 (APOE4) gene, which is associated with an increased risk of developing Alzheimer's.
About half of people with Alzheimer's disease carry the APOE4 gene, which can be inherited from either parent, said Schneider, professor of psychiatry and the behavioral sciences and professor of neurology. About 25 percent of the population carries one copy of the APOE4 gene, and about 2 to 3 percent of the population carries two copies, having received one from each parent. To qualify for the study, participants must have two copies of the gene.
Delay the disease
Qualifying participants may randomly receive either a vaccine, oral medication, placebo vaccine or placebo oral medication. Both the vaccine and oral medication target —the main component in amyloid plaques in the brain and a culprit in Alzheimer's—in two different ways: The vaccine helps the body develop antibodies against amyloid beta, while the oral medication blocks an enzyme that creates amyloid beta. Participants may receive the study medications for five to eight years.
"If we are able to show that the vaccine or oral is effective at delaying Alzheimer's among people at higher risk, then this would strongly imply that we are on the right track for developing treatments," Schneider said. "If we can delay the onset of Alzheimer's by five years, for example, the incidence of the illness would drop by half. It would also give individuals five more years without symptoms of the illness."
Should the vaccine or prove to be effective in people with two copies of the APOE4 gene, then it would likely also be effective for other people at risk for Alzheimer's, according to Schneider.
"Our clinician-scientists have been actively involved in clinical drug development for Alzheimer's for more than 30 years," said Rohit Varma, dean of the Keck School of Medicine. "This study is a reflection of our continued efforts to conquer one of the greatest health challenges of our time."
For information about how to participate in the study, contact Nadine Diaz at (323) 442-7600 or ndiaz@usc.edu.
Provided by: University of Southern California search and more info website