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.

Monday, September 7, 2015

At 50, Each Body Mass Index Unit Increase Hastens Alzheimer’s 6.7 Months

At 50 I was in fantastic shape, hell I was carrying canoes and gear on 1.5 mile portages.  So the question that our researchers need to answer; What are our chances of getting Alzheimers post-stroke and what can we do to prevent that? A very simple question but our fucking failures of stroke associations will not even attempt to answer that.
http://www.biosciencetechnology.com/articles/2015/09/50-each-body-mass-index-unit-increase-hastens-alzheimers-67-months?
Cynthia Fox, Science Writer

Obesity, once seen as sign of wealth, actually hastens dementia: The Tuscan General Alessandro del Borro, attributed to Charles Mellin, 1645[175] (Wikimedia)
Obesity, once seen as sign of wealth, actually hastens dementia: The Tuscan General Alessandro del Borro, attributed to Charles Mellin, 1645[175] (Wikimedia)
A new Molecular Psychiatry study has found a robust relationship between obesity at age 50—as measured by body mass index (BMI)—and both earlier age, and severity, of Alzheimer’s disease (AD). In particular, a National Institutes of Aging (NIA) team found that each unit increase in midlife BMI predicts earlier onset of AD by 6.7 months.
“This paper reports analysis of a very well-characterized cohort to identify how midlife obesity influences risk of late-life dementia,” Kaarin Anstey, Ph.D., F.A.S.S.A., told Bioscience Technology. Anstey is director of the Australian National University Dementia Collaborative Research Centre.
“Importantly, the authors showed that high BMI in midlife predicted age of onset of dementia. This is a novel finding. Before this article, we knew that high BMI increased the overall risk of dementia, but we did not know that it also meant that people would develop the disease at a younger age.  Another important finding was that the effect of BMI was independent of genetics.” Anstey was uninvolved in the new study.
“This article touches on an extremely important health topic, the effects of the epidemic obesity of western populations, in particular the U.S.,” University of Gothenburg psychologist Linda Hassing, Ph.D., told Bioscience Technology. “I believe the findings of this study reflect a real scenario. Overweight and obesity are significantly contributing cases to dementia, both AD and vascular dementia, [and] overweight and obesity will bring on an earlier onset of dementia.” Hassing was also uninvolved with the study.
“Our research specifically shows that midlife obesity lowers the age at onset of AD [and] accelerates AD development,” said senior author Madhav Thambisetty, M.D., Ph.D., chief of the NIA’s Unit of Clinical and Translational Neuroscience. Novel, he said, was “the amount of brain pathology” his team found associated with mid-life BMI, and the fact “that midlife BMI may have long lasting effect on the age at onset of AD.”
BMI’s predictive power
The NIA team looked at Baltimore Longitudinal Study on Aging (BLSA) data on 1,394 cognitively healthy people who underwent neuropsychological assessments on average every two years for some 14 years. Thambisetty’s team analyzed the link between BMI at age 50, and AD onset.
Out of this pool, 142 people developed AD. In these people, a higher midlife BMI was associated with earlier AD onset. Also, among 191 autopsy results, higher BMI at midlife was linked to more severe AD-related neurofibrillary amyloid.



Madhav Thambisetty, M.D., Ph.D., chief of the NIA’s Unit of Clinical and Translational Neuroscience:
Madhav Thambisetty, M.D., Ph.D., chief of the NIA’s Unit of Clinical and Translational Neuroscience:
The study did not explore mechanisms. Needed are larger studies, looking at the link at a variety of ages, the team reported, to get even more precise. “Understanding how risk factors in midlife may accelerate the onset of AD in later life is important in our efforts to develop interventions/treatments that may delay the onset of AD,” Thambisetty told Bioscience Technology. “Although being overweight or obese in midlife is known to increase the risk of AD, we do not yet understand how it may affect the age when the disease first begins. Another important question is whether midlife obesity affects the amount of brain pathology due to AD.”
Both questions were answered by the study to a certain degree. One unit of BMI was found to advance AD by 6.7 months, and considerable BMI affects severity of AD’s physical ravages on the brain.
“We would like to confirm these findings in larger studies with a wider range of BMI values, and in younger individuals,” Thambisetty said. “This will be important to conclusively determine whether there are certain BMI values and/or ages when the relationships with age-at-onset, and brain pathology, are especially strong.”
Anstey agrees more studies are needed. “The results again provide support for the idea that modifying BMI in middle-aged adults may modify dementia risk,” she told Bioscience Technology. “The work does need to be replicated in other studies, and further research is required to find out if high BMI in early adulthood, and even in childhood, may affect dementia risk.”
Minor reservation
Hassing introduced a “minor” reservation. Although the BLSA source of the data lends credibility to the work given its “scientific reliability in terms of research design and data collection, use of a community-dwelling sample, extensive follow-up time, and accuracy of the methods such as the dementia diagnoses, for this particular article they did not actually measure BMI at age 50,” she said. “They used statistical methods to derive a measure that estimates BMI at age 50.”
On the other hand, she said, “a perfect study design that examines the association between BMI and dementia would need to follow a big-sized population-based sample from midlife up to old age, a very time consuming and expensive project that, to my knowledge, has not yet been enforced.”
Regarding the accuracy of statistical measurements, Thambisetty called the comment on statistical measurement accuracy “a very good question…. In our sample of 1,394 participants in the BLSA, we had 8061 actual BMI measurements, recorded every year or every two years, during the course of follow up. Thus, each participant had, on average, almost six measurements of BMI throughout their participation in the study. The value of BMI at age 50 is then derived from all available actual, repeated BMI measurements using well-established statistical methods. This method also allows us to assess and account for the reliability of BMI estimates for each participant at age 50 years.”
Otherwise, he agreed, “in order to conclusively establish whether there is a `threshold’ of BMI value above which the associations with onset age and brain pathology are especially strong, and whether there is a specific age above which the associations with AD onset and brain pathology become important, it would be essential to follow a much larger sample representing a wider range of BMI values and ages.”
April Lancet study
A June Lancet study came to a surprisingly different conclusion. Underweight people in mid-life seemed more at risk for dementia.
Thambisetty told Bioscience Technology it is key to compare characteristics of participants across studies “when assessing results that seem contradictory. Our sample in the BLSA is a predominantly healthy, highly educated sample. All participants are cognitively normal at enrollment, and are assessed by detailed neuropsychological evaluations with diagnoses of AD made according to standardized criteria.
The Lancet study, on the other hand, is comprised of clinical records from patients who went in to see their primary physician for medical reason(s). This database is called the Clinical Practice Research Datalink (CPRD). It represents a very heterogeneous group with a variety of co-morbid illnesses that made them go in to see their doctor.  We are currently working with collaborators in the UK to analyze the CPRD data from which the Lancet results were obtained. We believe that a careful re-analysis of this data, accounting for the effects of obesity on risk of mortality, will be important before drawing conclusions about obesity and AD risk in this sample. This work is currently in progress.”
An online BMI calculator is here

Ask your doctor, 'Is nature right for you?'

A serious question. What the hell is your doctor doing to make sure you get some?
Prescription strength nature
For these reasons:

Shinrin-yoku Forest Therapy


Nature experience reduces rumination and subgenual prefrontal cortex activation


Glancing at greenery can boost concentration levels


5 Scientific Reasons A Beach Vacation Is Necessary For Your Health


The Cognitive Benefits of Interacting With Nature

Does your doctor know about ANY of these?

Sunday, September 6, 2015

'You never suffer from a money problem, you always suffer from an idea problem."

My fortune from a Japanese, Chinese, Thai restaurant in NYC the other night. Well money is still ok even after losing half the assets in the divorce.  My idea problem is that I think way too large and I don't have the infrastructure or minions to accomplish those ideas.

Monkey 'brain net' raises prospect of human brain-to-brain connection

I can easily see applications for stroke survivors, although this is probably at least a hundred years off if we get a great stroke association. Never if the existing fucking failures of stroke associations stay around sucking the funds that could be used to solve all the fucking problems in stroke.
http://www.theguardian.com/science/2015/jul/09/monkey-brain-net-raises-prospect-of-human-brain-to-brain-connection
Scientists have linked together the brains of three monkeys, allowing the animals to join forces and control an avatar arm, in research that raises the prospect of direct brain-to-brain interfaces in humans.
In a second experiment, the brains of four rats were wired together in a “brain net”, enabling the rodents to synchronise their neuronal activity and collaboratively solve a simple weather forecasting problem that individual rats struggled to complete.
The experiments, which have echoes of the Borg, a sinister alien collective in Star Trek, challenge the notion that our minds will always be ultimately isolated from those of others.
Miguel Nicolelis, the Duke University scientist behind the work, has previously pioneered the development of brain-machine interfaces that could allow amputees and paralysed people to directly control prosthetic limbs and exoskeletons. His latest advance may have clinical benefits in brain rehabilitation, he predicts, but could also pave the way for “organic computers” - collectives of animal brains linked together to solve problems.
“Essentially we created a super-brain,” he said. “A collective brain created from three monkey brains. Nobody has ever done that before.”
He dismissed comparisons with science fiction plots, however, saying: “We’re conditioned by movies and Hollywood to think that everything related to science is dangerous and scary. These scary scenarios never crossed my mind and I’m the one doing the experiments.”
Anders Sandberg, a neuroethics researcher at the University of Oxford, said the work was the most convincing demonstration yet that brains can be linked together in direct communication. “People have claimed digital telepathy in various cool demos, but it’s mostly been total hype,” he said. “I’m quite impressed by this. It has a high ‘gosh’ factor.”
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In the first study, scientists fitted three rhesus macaque monkeys with arrays that could record electrical activity from hundreds of neurons in the motor region of the brain.
The monkeys learnt, independently, to control the 3D movements of an avatar arm shown on a digital display in front of them, just by imagining moving it. The monkeys were then given joint control of the arm, with each monkey able to control two out of three dimensions (for instance, along the x- and y-axis) and their activity made a 50% contribution to each.
Although their brains were not directly wired together, the monkeys intuitively started to synchronise their brain activity, allowing them to move the arm collaboratively to a reach for a virtual ball on the screen.
The system appeared to work, even if one of the three monkeys was temporarily distracted. “Even if one monkey dropped out in one trial, the brain net is resilient,” said Nicolelis. “Imagine if you had, not three, but a million. That would be extremely resilient.”
In a second paper, also published in the journal Scientific Reports, the scientists directly linked the brains of rats together via two-way electrical connections that allowed the scientists to both deliver stimulus to neurons and read out electrical activity.
In one experiment, an electrical impulse was delivered to the brain of one rat, and the other rats learnt to synchronise their brain activity, mimicking the first rat’s brain response. In a sense, they were experiencing what the first rat felt, second-hand.
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In another demonstration, pulses of stimulation that increased or decreased were delivered to the brains of individual rats, representing temperature and barometric pressure information. The rats were able to combine the information to produce a collective output that predicted an increased or decreased chance of rain. Rats scored better on this task when they were linked as a “brain net”, than when individual rats tried to combine the two pieces of initial information – temperature and pressure – to perform the simple calculation alone.
The scientists said that in the future, the concept might be extended to produce neurally connected “swarms” of rats with collective intelligence.
Nicolelis said that in the long-term the work could have “tremendous benefits” for brain rehabilitation. After suffering a stroke, for instance, language abilities might be able to be restored more quickly if a patient’s brain was retrained by directly synchronising with the language regions of the brain of a healthy person. In humans, the link could potentially be made non-invasively using electrodes on the scalp, however.
But he added it was unlikely that humans would ever be able to directly share complex mental experiences. “You’re not going to share your emotions or personality to a brain-net,” he said. “These are not reducible to a digital algorithm. You can’t reproduce these individual human attributes.”
Ultimately, people may also decide that wiring themselves up with others is not entirely desirable. “There may be special instances where you’d want a long-term connection with someone – like a married couple or a military platoon,” said Sandberg. “But there’s no guarantee that brain-to-brain interfaces will be a sensible thing in practice. There’s something to be said for neural privacy.”

Synchronized brain waves enable rapid learning

So have your doctor create/steal a protocol that does this. We need rapid learning, why isn't your doctor helping you get better? Or is she/he WAITING FOR SOMEONE ELSE TO SOLVE THE PROBLEM

Synchronized brain waves enable rapid learning



The human mind can rapidly absorb and analyze new information as it flits from thought to thought. These quickly changing brain states may be encoded by synchronization of brain waves across different brain regions, according to a new study from MIT neuroscientists.
The researchers found that as monkeys learn to categorize different patterns of dots, two brain areas involved in learning — the prefrontal cortex and the striatum — synchronize their brain waves to form new communication circuits.
“We’re seeing direct evidence for the interactions between these two systems during learning, which hasn’t been seen before. Category-learning results in new functional circuits between these two areas, and these functional circuits are rhythm-based, which is key because that’s a relatively new concept in systems neuroscience,” says Earl Miller, the Picower Professor of Neuroscience at MIT and senior author of the study, which appears in the June 12 issue of Neuron.
There are millions of neurons in the brain, each producing its own electrical signals. These combined signals generate oscillations known as brain waves, which can be measured by electroencephalography (EEG). The research team focused on EEG patterns from the prefrontal cortex —the seat of the brain’s executive control system — and the striatum, which controls habit formation.
The phenomenon of brain-wave synchronization likely precedes the changes in synapses, or connections between neurons, believed to underlie learning and long-term memory formation, Miller says. That process, known as synaptic plasticity, is too time-consuming to account for the human mind’s flexibility, he believes.
“If you can change your thoughts from moment to moment, you can’t be doing it by constantly making new connections and breaking them apart in your brain. Plasticity doesn’t happen on that kind of time scale,” says Miller, who is a member of MIT’s Picower Institute for Learning and Memory. “There’s got to be some way of dynamically establishing circuits to correspond to the thoughts we’re having in this moment, and then if we change our minds a moment later, those circuits break apart somehow. We think synchronized brain waves may be the way the brain does it.”
The paper’s lead author is former Picower Institute postdoc Evan Antzoulatos, who is now at the University of California at Davis.
Humming together
Miller’s lab has previously shown that during category-learning, neurons in the striatum become active early, followed by slower activation of neurons in the prefrontal cortex. “The striatum learns very simple things really quickly, and then its output trains the prefrontal cortex to gradually pick up on the bigger picture,” Miller says. “The striatum learns the pieces of the puzzle, and then the prefrontal cortex puts the pieces of the puzzle together.”
In the new study, the researchers wanted to investigate whether this activity pattern actually reflects communication between the prefrontal cortex and striatum, or if each region is working independently. To do this, they measured EEG signals as monkeys learned to assign patterns of dots into one of two categories.
At first, the animals were shown just two different examples, or “exemplars,” from each category. After each round, the number of exemplars was doubled. In the early stages, the animals could simply memorize which exemplars belonged to each category. However, the number of exemplars eventually became too large for the animals to memorize all of them, and they began to learn the general traits that characterized each category.
By the end of the experiment, when the researchers were showing 256 novel exemplars, the monkeys were able to categorize all of them correctly.
As the monkeys shifted from rote memorization to learning the categories, the researchers saw a corresponding shift in EEG patterns. Brain waves known as “beta bands,” produced independently by the prefrontal cortex and the striatum, began to synchronize with each other. This suggests that a communication circuit is forming between the two regions, Miller says.
“There is some unknown mechanism that allows these resonance patterns to form, and these circuits start humming together,” he says. “That humming may then foster subsequent long-term plasticity changes in the brain, so real anatomical circuits can form. But the first thing that happens is they start humming together.
A little later, as an animal nailed down the two categories, two separate circuits formed between the striatum and prefrontal cortex, each corresponding to one of the categories.
“This is the first paper that provides data suggesting that coupling in the beta-band between prefrontal cortex and striatum may play a key role in category-formation. In addition to revealing a novel mechanism involved in category-learning, the results also contribute to better understanding of the significance of coupled beta-band oscillations in the brain,” says Andreas Engel, a professor of physiology at the University Medical Center Hamburg-Eppendorf in Germany.
“Expanding your knowledge”
Previous studies have shown that during cognitively demanding tasks, there is increased synchrony between the frontal cortex and visual cortex, but Miller’s lab is the first to show specific patterns of synchrony linked to specific thoughts.
Miller and Antzoulatos also showed that once the prefrontal cortex learns the categories and sends them to the striatum, they undergo further modification as new information comes in, allowing more expansive learning to take place. This iteration can occur over and over.
“That’s how you get the open-ended nature of human thought. You keep expanding your knowledge,” Miller says. “The prefrontal cortex learning the categories isn’t the end of the game. The cortex is learning these new categories and then forming circuits that can send the categories down to the striatum as if it’s just brand-new material for the brain to elaborate on.”
In follow-up studies, the researchers are now looking at how the brain learns more abstract categories, and how activity in the striatum and prefrontal cortex might reflect that type of abstraction.
The research was funded by the National Institute of Mental Health.

Shinrin-yoku Forest Therapy

There is absolutely no reason your doctor and therapists can't get you into a natural area for all its attendant benefits. Great links to research since your doctor won't do anything about this unless you Call the president and demand that your doctors get up-to-date on research. Ok, the life force might be bogus but the rest is good.
http://www.shinrin-yoku.org/shinrin-yoku.html
Shinrin-yoku is a term that means "taking in the forest atmosphere" or "forest bathing." It was developed in Japan during the 1980s and has become a cornerstone of preventive health care and healing in Japanese medicine. Researchers primarily in Japan and South Korea have established a robust body of scientific literature on the health benefits of spending time under the canopy of a living forest. Now their research is helping to establish shinrin-yoku and forest therapy throughout the world.

The idea is simple: if a person simply visits a natural area and walks in a relaxed way there are calming, rejuvenating and restorative benefits to be achieved.

We have always known this intuitively. But in the past several decades there have been many scientific studies that are demonstrating the mechanisms behind the healing effects of simply being in wild and natural areas. (some of this research is available here). For example, many trees give off organic compounds that support our “NK” (natural killer) cells that are part of our immune system's way of fighting cancer.
The scientifically-proven benefits of Shinrin-yoku include:
  • Boosted immune system functioning, with an increase in the count of the body's Natural Killer (NK) cells.
  • Reduced blood pressure
  • Reduced stress
  • Improved mood
  • Increased ability to focus, even in children with ADHD
  • Accelerated recovery from surgery or illness
  • Increased energy level
  • Improved sleep
Just as impressive are the results that we are experiencing as we make this part of our regular practice:
  • Deeper and clearer intuition
  • Increased flow of energy
  • Increased capacity to communicate with the land and its species
  • Increased flow of eros/life force
  • Deepening of friendships
  • Overall increase in sense of happiness
Picture
Opening our senses to nature also develops our intuition. We learn to contact in new ways the world around us.
We recognize that forest therapy approaches such as Shinrin-yoku have roots in many cultures throughout history. John Muir wrote, “Thousands of tired, nerve-shaken, over-civilized people are beginning to find out that going to the mountains is going home. Wilderness is a necessity.” He is one of many people who we include when we think about the origins of the practice.

Our approach to Shinrin Yoku Forest Therapy combines leisurely walks on gentle paths under forest canopy with guided activities and meditations to help you open your senses, hone your intuition, and experience the forest as you never have before. We draw upon mindfulness meditation practices, and the techniques of deep nature connection mentoring. We also use the Way of Council for group discussions at several points along the walk, which helps participants learn from and teach other as we discuss what we are experiencing together. 

Saturday, September 5, 2015

One hand bandages

I bet your Occupational therapist doesn't know about this. I could have used this multiple times in the past nine years. Expensive but I'd have much less blood sprayed over my clothes.
http://www.duluthtrading.com/store/product/one-hand-bandages-85556.aspx?

The improvement effect of limited mental practice in individuals with poststroke hemiparesis: the influence of mental imagery and mental concentration.

I would disagree with the conclusions here since other research proves it works. But hell, ask your fucking doctor for guidance.
http://web.a.ebscohost.com/abstract?direct=true&profile=ehost&scope=site&authtype=crawler&jrnl=09155287&AN=109081614&h=XW%2f7NnVIHLiM5kocpwN1pO0hwP8YfSTXZXw%2fFozd8NnqikDzWHAwUDf8xglwSyb%2fEUJsdoRnaM7u1%2fmZqa1m8Q%3d%3d&crl=c&resultNs=AdminWebAuth&resultLocal=ErrCrlNotAuth&crlhashurl=login.aspx%3fdirect%3dtrue%26profile%3dehost%26scope%3dsite%26authtype%3dcrawler%26jrnl%3d09155287%26AN%3d109081614
  • Source: Journal of Physical Therapy Science . Aug2015, Vol. 27 Issue 8, p2641-2644. 4p.
  • Author(s): KATSUHITO NAGANO; YUMI NAGANO
  • Abstract: [Purpose] This study examined whether limited mental practice improves the motor performance of poststroke individuals with hemiparesis. [Subjects] Twenty-three participants with poststroke hemiparesis (40-82 years of age) participated in this study. [Methods] The subjects were divided into four groups with respect to a dart-throwing task: the no-practice, physical practice only, mental practice only, and mental and physical practice groups. The groups were compared in terms of gains in motor performance, mental imagery vividness, and level of concentration during mental practice. 
  • [Results] No statistically significant difference was found for gains in motor performance among groups, and there was no correlation between imagery vividness and motor performance gains. However, a correlation was found between gains in motor performance and mental concentration during mental practice. [Conclusion] The results suggested that limited mental practice for individuals with poststroke hemiparesis may not improve motor performance. However, a higher degree of concentration during mental practice may improve motor performance.
  • Copyright of Journal of Physical Therapy Science is the property of International Press Editing Center Incorporation and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.

Effect of discontinuation of antihypertensive treatment in elderly people on cognitive functioning—the DANTE study Leiden: a randomized clinical trial

Have your doctor analyze this result as compared to this:

High blood pressure linked to reduced Alzheimer's risk, meds may be reason

Well your doctor should know this stuff otherwise why the hell are you seeing them? I expect my doctors to know more than I do and so far that is not the case.

Effect of discontinuation of antihypertensive treatment in elderly people on cognitive functioning—the DANTE study Leiden: a randomized clinical trial

Observational studies indicate that lower blood pressure (BP) increases risk for cognitive decline in elderly individuals. Older persons are at risk for impaired cerebral autoregulation; lowering their BP may compromise cerebral blood flow and cognitive function. To assess whether discontinuation of antihypertensive treatment in older persons with mild cognitive deficits improves cognitive, psychological, and general daily functioning. In older persons with mild cognitive deficits, discontinuation of antihypertensive treatment did not improve cognitive, psychological, or general daily functioning at the 16–week follow–up.

Methods

  • A community–based randomized clinical trial with a blinded outcome assessment at the 16–week follow–up was performed at 128 general practices in the Netherlands.
  • A total of 385 participants 75 years or older with mild cognitive deficits (Mini–Mental State Examination score, 21–27) without serious cardiovascular disease who received antihypertensive treatment were enrolled in the Discontinuation of Antihypertensive Treatment in Elderly People (DANTE) Study Leiden from June 26, 2011, through August 23, 2013 (follow–up, December 16, 2013).
  • Intention–to–treat analyses were performed from January 20 through April 11, 2014.
  • Discontinuation (n=199) vs continuation (n=186) of antihypertensive treatment (allocation ratio, 1:1).
  • Change in the overall cognition compound score.
  • Secondary outcomes included changes in scores on cognitive domains, the Geriatric Depression Scale–15, Apathy Scale, Groningen Activity Restriction Scale (functional status), and Cantril Ladder (quality of life).

Results

  • Compared with 176 participants undergoing analysis in the control (continuation) group, 180 in the intervention (discontinuation) group had a greater increase (95% CI) in systolic BP (difference, 7.36 [3.02 to 11.69] mm Hg; P=.001) and diastolic BP (difference, 2.63 [0.34 to 4.93] mm Hg; P=.03).
  • The intervention group did not differ from the control group in change (95% CI) in overall cognition compound score (0.01 [-0.14 to 0.16] vs -0.01 [-0.16 to 0.14]; difference, 0.02 [-0.19 to 0.23]; P=.84).
  • The intervention and control groups did not differ significantly in secondary outcomes, including differences (95% CIs) in change in compound scores of the 3 cognitive domains (executive function, -0.07 [-0.29 to 0.15; P=.52], memory, 0.08 [-0.12 to 0.29; P=.43], and psychomotor speed, -0.85 [-1.72 to 0.02; P=.06]), symptoms of apathy (0.17 [-0.65 to 0.99; P=.68]) and depression (0.14 [-0.20 to 0.48; P=.41]), functional status (-0.72 [-1.52 to 0.09; P=.08]), and quality–of–life score (-0.09 [-0.34 to 0.16; P=.46]).
  • Adverse events were equally distributed.

 

What Women Don't Know About Stroke Could Kill Them (Op-Ed)

And what your doctor doesn't know about stroke rehabilitation(getting you back to 100%) means that you will likely be disabled for the rest of your life.
according to their stroke risk calculator I was at low risk for getting a stroke.
http://news.yahoo.com/women-dont-know-stroke-could-kill-them-op-204247059.html
Dr. Diana Greene-Chandos, neurologist and director of neuroscience critical care at Ohio State's Wexner Medical Center, contributed this column to Live Science's Expert Voices: Op-Ed & Insights.
Too few women know the female-specific risks and symptoms of a stroke, and it can have devastating consequences. I've seen it for years in my practice as a neurologist, and a recent national survey only underscores the same troubling truth.
The survey, commissioned and released by our hospital, The Ohio State University Wexner Medical Center, went to 1,000 women nationwide and found that only 11 percent could correctly identify pregnancy, lupus, migraine headaches, oral contraception or hormone replacement therapy as female-specific risks for stroke.html.
That's an alarming statistic given the vast number of women who have a connection to one or more of those risk factors. Unfortunately, many women think of stroke as a "men's health issue," but it is the third-highest cause of death among females in the United States, and claims more than 80,000 women each year, according to the National Stroke Association.
Spotting the symptoms
The symptoms of a stroke can be different for women than men, though few females in the survey were able to pinpoint some of those differences. Only 10 percent of women, for example, knew that females can experience hiccups and atypical chest pain during a stroke.
Awareness of particular early warning signs is important during a stroke because many women might assume they have indigestion and delay seeking medical attention. This can have serious consequences. Only within the first three hours after the onset of stroke is emergency treatment with clot-busting drugs a viable option. Women often miss this window because they don't know what early warning signs to watch for.
The signs of stroke in women include:
  • Hiccups
  • Dizziness
  • Chest pain
  • Headache
  • Body numbness, with one side being more numb than the other
Some symptoms, however, are the same for both women and men. These include:
  • Facial droop or uneven smile
  • Weakness that involves the arm and leg on the same side of the body
  • Slurred speech or difficulty speaking or understanding
If you experience any of these symptoms, don’t delay treatment. Call 911 immediately.
How women heal from stroke
The survey also found that nearly half of all women don't know the challenges females can face after a stroke. Things like nerve damage and paralysis can cause issues with swallowing, but many women who survive a stroke also suffer from depression, which often deters them from the idea of attending rehab as early and as often as they should.
Doctors have a long way to go to educate women about stroke, (they have even longer to go to get survivors back to normal and I bet even this doctor doesn't know how to get patients rehabbed) including the risks and symptoms unique to them. All of us, men and women, need to know that smoking, a lack of exercise and blood pressure above 140/90 can raise our risk of stroke. (Nowhere in here is there ANY responsibility of doctors to know how to treat patients recovering from stroke.)  It's obviously WAITING FOR SOMEONE ELSE TO SOLVE THE PROBLEM

You're fucking screwed because there is no one in the world that has any clue how specifically to get anyone recovered.  In general the answer is neuroplasticity and neurogenesis, but no one knows how to replicate those on demand.
Hemoglobin A1C levels above 5.7 can also raise the likelihood of stroke. When no other risk factors are present, so do LDL (bad cholesterol) levels greater than 100. For those with diabetes, the risks are greater and those individuals will need to be more aggressive. When coupled with diabetes, any A1C level above 7.0 and an LDL cholesterol level greater than 70 drive up the risk of stroke.
There are some studies that suggest lowering LDL too much may increase the risk of hemorrhagic stroke, but this is not a guideline nor is there a target number. When there are no additional risk factors present, an LDL level greater than 100 increases a person’s risk of stroke.
As our society ages, we expect the number of strokes will continue to climb. It's imperative that all of us, especially women, better understand the risks and symptoms so rapid treatment can reduce complications and improve survival.
To assess your own risk for stroke, check out the Wexner Medical Center's stroke assessment test.
Follow all of the Expert Voices issues and debates — and become part of the discussion — on Facebook, Twitter and Google+. The views expressed are those of the author and do not necessarily reflect the views of the publisher. This version of the article was originally published on Live Science.

Friday, September 4, 2015

"It's not worth doing my best"

This must be the mantra from our stroke medical leadership. That would require expending a lot of energy and intellectual capital. And the result would only be to help stroke survivors. Obviously not worth doing. You're fucking screwed if you have a stroke right now. Don't let your doctors off the hook for their lack of getting you fully recovered.
From Seth Godin.

On doing your best 

It's a pretty easy way to let ourselves (or someone else) off the hook. "Hey, you did your best."
But it fails to explain the improvement in the 100-meter dash. Or the way we're able to somehow summon more energy and more insight when there's a lot on the line. Or the tremendous amount of care and love we can bring to a fellow human who needs it.
By defining "our best" as the thing we did when we merely put a lot of effort into a task, I fear we're letting ourselves off the hook.
In fact, it might not require a lot of effort, but a ridiculous amount of effort, an unreasonable amount of preparation, a silly amount of focus... and even then, there might be a little bit left to give.
It's entirely possible that it's not worth the commitment or the risk or the fear to go that far along in creating something that's actually our best. But when we make that compromise, we should own it. "It's not worth doing my best" is actually more honest and powerful than failing while being sort of focused.

 

Flight fun

I was supposed to leave LaGuardia airport at 6:30 pm leaving me an hour layover in Detroit to catch the next flight. 3 of us took a taxi and arrived at 3pm to make sure we didn't get caught in afternoon rush hour traffic. On the way there I got a text that my flight was delayed by 45 minutes meaning that there was no way to get on the final flight on time. Then I got another text telling me I had been rescheduled to a 3:35 flight to Columbus, then Detroit,  then Lansing.  Since this was a totally different flight I now needed to be in a different terminal which the gate agent called on one of the wheelchair service people and I got whisked thru the TSA line in no time. Barely made it to the gate on time to find out it's delayed 15 minutes, then another 15 minutes as the plane needs cooling down.  We board, sit there 10 minutes and have to deplane because the cooler is not working properly. 45 minutes later we board again.  Now I only have 30 minutes to catch my next flight. Land at 7pm in Columbus.  Rush to my gate. The previous flight to Detroit from 4:51 has not left yet. It seems thunderstorms in Detroit have delayed everything. After the storms clear Detroit, lightning at Columbus prevents the ground crew from getting out there. We finally board the plane around 9:30, about the time my flight to Lansing from Detroit is to take off. That final flight is delayed till 11:02 so it may be possible to still make it. But as we are taxiing to the gate in Detroit I can see the gate where the Lansing plane is supposed to be is already empty. So I now have a 10am flight to Lansing in the morning. I'm spending the night at the airport since I'm too cheap to get a hotel and I'm not sure work would pick up the expense. No idea where my luggage is. I'll be flying back to New York on Labor day to work there Tues., Wed., Thu. And I'll be staying in a totally different area at a different hotel. Time to get completely lost multiple more times. Currently 1:49 am Eastern time. Life is good. We had a great plane turbulence drop on the way to Detroit, everyone got excited. One guy thought for sure we were going down.

Getting lost

Getting lost in NYC once again. I needed to be at 1 New York Plaza by 9am. My hotel is at the intersection of Nassau and Maiden Lane. Instead of taking Nassau all the way down to the waterfront I took Maiden Lane and ended up 5 blocks away. Sweating and swearing away because I'm hauling my suitcase around in 78 degree heat. My ability to use and understand google maps on my phone isn't working.  I'm still old school enough that I prefer paper maps even though right now that is totally impossible to use one-handed. Still made it in time.

Entitlement

Overheard two cases of extreme entitlement while waiting out a flight delay at LaGuardia. One guy seemed to think that all of Delta needed to fix his personal flight delays but he would be pacified by 30,000 miles added to his account.  The other guy wanted to personally talk to one of the programers who was working on one of his smartphone apps.
NY seems to a hellhole of entitled bastards.Glad I don't live there.

Thursday, September 3, 2015

Mice in an enriched environment learn more flexibly because of adult hippocampal neurogenesis

Just what the hell is it going to take to get your doctor to create an enriched environment in your hospital room? A two by four upside the head? Because nothing else seems to be working. This would be so fucking easy to implement, buy hanging mobiles that babies have above their cribs and add music.
http://onlinelibrary.wiley.com/doi/10.1002/hipo.22520/abstract
  1. Alexander Garthe1,2,
  2. Ingo Roeder3 and
  3. Gerd Kempermann1,2,*
DOI: 10.1002/hipo.22520

SEARCH

Keywords:

  • hippocampus;
  • plasticity;
  • stem cells;
  • memory;
  • environmental enrichment;
  • exercise

Abstract

We here show that living in a stimulus-rich environment (ENR) improves water maze learning with respect to specific key indicators that in previous loss-of-function experiments have been shown to rely on adult hippocampal neurogenesis. Analyzing the strategies employed by mice to locate the hidden platform in the water maze revealed that ENR facilitated task acquisition by increasing the probability to use effective search strategies. ENR also enhanced the animals' behavioral flexibility, when the escape platform was moved to a new location. Treatment with temozolomide, which is known to reduce adult neurogenesis, abolished the effects of ENR on both acquisition and flexibility, while leaving other aspects of water maze learning untouched. These characteristic effects and interdependencies were not seen in parallel experiments with voluntary wheel running (RUN), a second pro-neurogenic behavioral stimulus.
Since the histological assessment of adult neurogenesis is by necessity an end-point measure, the levels of neurogenesis over the course of the experiment can only be inferred and the present study focused on behavioral parameters as analytical endpoints. Although the correlation of physical activity with precursor cell proliferation and of learning and the survival of new neurons is well established, how the specific functional effects described here relate to dynamic changes in the stem cell niche remains to be addressed. Nevertheless, our findings support the hypothesis that adult neurogenesis is a critical mechanism underlying the beneficial effects of leading an active live, rich in experiences. This article is protected by copyright. All rights reserved.
Get PDF (1715K)

New Research Says Cerebellum Contributes to Creativity

What is your doctor doing to make sure your cerebellum damage is alleviated via an efficacious stroke protocol? ANYTHING AT ALL?
http://www.visualnews.com/2015/08/18/new-research-says-cerebellum-contributes-to-creativity/
by Katy French
Whether it’s electrical stimulation of the brain, taking a walk, or doing something boring, scientists are constantly looking for ways to help us be more creative. Neuroscientists are particularly interested in which areas of the brain contribute to or control creativity, and new research is giving us a little more insight. A new study by Stanford’s School of Medicine and the Hasso Plattner Institute of Design has found an unexpected link between creativity and the cerebellum, the part of the brain that controls movement.  Cerebellum_animation_small
This part of the brain has never been recognized as contributing to the creative process, but it turns out that it does play a part. For the study, researchers devised a method to test creativity—without explicitly telling participants that they were supposed to be creative—and monitored brainwave activity to identify what areas of the brain were being activated.
Participants were given two tasks: Visually depict certain words (a la Pictionary), such as “vote” or “salute,” and draw a zigzag line (a task that requires motor skills but not much creativity). While they performed the tasks, participants’ brains were monitored via MRI scans. Once the drawings were completed, participants were asked to rate how difficult the words they were given to draw were (to give researchers a sense of perceived difficulty). After the experiment, researchers analyzed and rated the drawings for creativity according to specific criteria, including accuracy of depiction, number of elements in the drawing, how elaborate or original the drawing was, etc.
What they found was surprising. Participants’ responses tracked with brainwave activity, meaning those who perceived a word to be more difficult exhibited higher activity in the left prefrontal cortex, an executive-function center responsible for attention and evaluation. But those who had produced more creative drawings exhibited low activity in the same center. The cerebellum was also particularly active for participants whose drawings were more creative—surprising as it has generally been thought to be responsible only for motor movement. In short, just drawing the zigzag lines didn’t produce nearly as much brain activity as the creative drawings did. Even more interestingly, more activity in certain areas signified a decrease in creativity.
“We found that activation of the brain’s executive-control centers — the parts of the brain that enable you to plan, organize and manage your activities — is negatively associated with creative task performance,” says Allan Reiss, MD, professor of radiology and of psychiatry and behavioral sciences.
“As our study also shows, sometimes a deliberate attempt to be creative may not be the best way to optimize your creativity,” Reiss says. “While greater effort to produce creative outcomes involves more activity of executive-control regions, you actually may have to reduce activity in those regions in order to achieve creative outcomes.”
What does that really mean? If you want to be more creative, don’t think so hard.
We’re down with that.

Clue to Brain Regeneration Discovered in Lab Mice

Fascinating stuff. If we had anything close to a fucking decent stroke association this would be added to one of the strategies requiring followup and foundation grants to get researchers to study this in humans. This is so god-damned brain dead simple. But I don't think we have anyone in the stroke medical leadership that has two functioning neurons. You're fucking screwed if you have a stroke anytime in the next 50 years.
More wonderful stuff from the Dana Foundation.
http://dana.org/News/Clue_to_Brain_Regeneration_Discovered_in_Lab_Mice/


A salamander can lose a limb or an eye and grow it back, nerves and all. A gecko can detach its tail on purpose—a great way to spoof a pursuing predator—and a new one will sprout in weeks. A zebrafish can regenerate missing parts of its heart and brain. Unfortunately we mammals just aren’t very good at regrowing lost bits.
Medicine would be transformed if we could find a way to surmount this limitation, particularly in the central nervous system (CNS), where regeneration is heavily restricted.
Among the more promising leads turned up recently is a finding from Harvard researchers, published online in May, that hints at a way to boost the regeneration capacity of CNS axons—nerve fibers that are often damaged in brain injuries and neurodegenerative diseases. Therapies that exploit the new finding are years away at best, but might end up being applicable to a variety of common, debilitating conditions, from strokes to Alzheimer’s and Parkinson’s.
“We’re pretty confident in this being quite a big deal,” says Harvard’s Michael Costigan, who was co-senior author of the study, along with Clifford J. Woolf.
The outlier
The researchers discovered the clue to improved axonal regeneration by looking at different strains of lab mice, to see which strain could regenerate its CNS axons better than the others. The nine strains selected are part of a set called the Collaborative Cross, which covers most of the genetic variation in mice and is commonly used by biologists to study the effects of gene mutations.
In an initial experiment, lead author Takao Omura harvested sensory neurons from the spines of the mice, and cultured the neurons in the presence of CNS myelin—a protein that normally sheathes CNS axons and also contains natural inhibitors of CNS axonal growth.
Sensory neurons like these have, so to speak, one foot in the central nervous system and the other in the peripheral nervous system, where regeneration is somewhat less restricted. A two-branched axon normally extends from the cell body of such a neuron, one being the “peripheral branch” that runs to its stimulus-sensing nerve end in the skin, bone, muscle, or other organ. The other, “central branch” sends sensory signals brainward via the spinal cord. The central branch is considered part of the CNS, yet it often does grow slightly longer after the peripheral branch is injured.
Omura and his colleagues found that one strain, known as CAST/Ei, stuck way out from the others in its ability to lengthen sensory neuron central branches following peripheral branch injury, and despite the presence of myelin-based growth inhibition.
“It was nothing like what you’d see in a normal lab mouse,” says Omura.
Image courtesy of Neuron, Omura et al
He obtained similar results when the neurons were cultured in the presence of chondroitin sulfate proteoglycans, a different set of axonal regrowth inhibitors normally produced in “glial scars” after CNS injury.
Remarkably, Omura found that in lab dish tests without CNS axon-regrowth inhibitors, the central branch axons of pre-injured sensory neurons grew longer in the other strains too, so that the growth seen in CAST/Ei mice was no longer dramatically greater. That result suggests that the key difference in CAST/Ei mice is not a broadly higher propensity for axonal growth, but a specific ability to overcome the growth-inhibiting environment of the adult CNS.
Moving beyond lab-dish tests, Omura conducted tests in live mice of spine damage, optic nerve crush, and stroke, and confirmed in each case that CAST/Ei neurons have an unusually strong ability to regrow their axons despite the inhibitory environment of the CNS, when they are pre-conditioned with a mild injury.
The average axonal regrowth in the CAST/Ei mice in these in vivo experiments, says Omura, “was at least several times what we saw in the C57BL/6 comparison strain.”
Is Activin the answer?
To find the source of this dramatically increased regenerative capacity, Omura and colleagues looked at neuronal gene expression patterns across the different strains. The gene whose expression seemed most tightly linked to CAST/Ei axonal regeneration in the presence of myelin turned out to be Inhba—which codes for a subunit of a protein called Activin.
Activin is involved in development, wound-healing, and other pro-growth functions. Prior studies have linked it to fin regeneration in zebrafish and tail regeneration in geckos.
Remarkably, levels of Inhba gene transcripts in sensory neurons jumped after injury only in the CAST/Ei mice, but not in other strains, and not in a rat that was also tested. That result suggested that CAST/Ei mice uniquely overproduce Activin after nerve injury, and the increased Activin signaling—possibly with other factors—somehow helps negate the usual growth-inhibitory environment.
To confirm the role of Activin signaling, the researchers blocked it in pre-conditioned, myelin-cultured neurons from the CAST/Ei mice, using an Activin receptor antagonist compound, and observed a major reduction in new axonal growth. Conversely, adding Activin proteins to myelin-cultured neurons from a more standard mouse strain caused ten times as many neurons to extend their axons, and boosted the average length of the new growth by a factor of nearly four. A preliminary test also indicated that Activin can have a similar growth-permitting effect in injured retinal neurons from rats.
Activin is part of a family of proteins that signal via the same set of receptors and have functions that aren’t fully understood. Intriguingly, the “fountain of youth” protein GDF11, recent results for which have drawn controversy—some say it is a regeneration booster, others a regeneration inhibitor—also appears to signal through Activin receptors.
Costigan says that he and his lab are now trying, “step by step,” to discover the precise mechanisms that confer a greater axonal regeneration capacity on CAST/Ei mice.
What makes CAST/Ei mice so special?
One of the questions raised by the findings is: how did the CAST/Ei mice end up with this striking capacity for CNS axon regeneration whereas the other tested strains don’t have it?
“I think it was just chance genetic variation that was fixed in that inbred strain,” says Greg Cox, a researcher at The Jackson Laboratory, which created the CAST/Ei strain and others used in the study.
Cox points out that inbred mouse strains often vary greatly in their genetic backgrounds, disease susceptibilities, behaviors, and so on—comparable to the variation seen in the human population.
Omura nevertheless wonders whether CAST/Ei mice are less unique than they seem. Most lab mouse strains are derived from long-domesticated “fancy mice”—essentially pets and show-animals. (Humans have been keeping mice as pets for centuries.) But the “founder” animals used to make the CAST/Ei strain were wild mice trapped by an American researcher in a grain warehouse in Chonburi, Thailand, around 1970. (CAST refers to the castaneous, or chestnut color of the animals, and Ei refers to Eva Eichler, the Jackson Laboratory researcher who bred the strain in 1971.)
“They do act wild,” says Costigan. “They jump around a lot and they’re very fast.”
Conceivably, greater axonal regeneration capacity was an important trait to have in the much harsher wild-mouse environment, and would be seen more frequently among wild-derived lab strains as well as in ordinary wild mice—if anyone decided to look.
“I’d love to test this hypothesis,” says Omura. “If we picked a wild mouse that’s living on the streets maybe it would have that phenotype–and maybe most lab mice have lost that phenotype.”
In any case, there may be more surprises to be found in CAST/Ei mice. Cox notes that his lab has been studying a mutation that causes a rare childhood motor neuron disease, spinal muscular atrophy with respiratory distress. When bred into the CAST/Ei mice, he says, the disease presentation, or phenotype, becomes significantly milder.
Similarly, Robert W. Burgess, another researcher at the Jackson Laboratory, has found that a genetic condition involving peripheral axon degeneration becomes milder when bred into the CAST/Ei strain. “It significantly downgrades the phenotype—they are less severe,” Burgess says.
Understanding how that works could be very useful, even if the CAST/Ei resistance to these neurological diseases is due only to a chance genetic variation.
“It’s a pretty powerful strain,” says Burgess.
- See more at: http://dana.org/News/Clue_to_Brain_Regeneration_Discovered_in_Lab_Mice/#sthash.wSYOHCSw.dpuf

A Simple Test Could Help Identify Thinking Problems

Something objective your doctor should be testing you on.
http://www.spring.org.uk/2015/09/a-simple-test-could-help-identify-thinking-problems.php?

Wednesday, September 2, 2015

I don't get email or comments

Considering how viciously I slam most stroke medical professionals and the stroke associations, it's even more appalling that they don't even know someone is criticizing them. What makes it worse is my assumption why they don't write to me is because they agree and are too chickenshit to acknowledge the failures in their professions.  Here's my address; write to me, you'll get a fair hearing based upon the facts you present; oc1dean@gmail.com
My 1.6 million visitors can't all be survivors. Tell me how YOU would fix the stroke medical profession or your stroke association. I can't do this alone.

Outed at my new gig

I'm on a new contract supporting Morgan Stanley, having to travel to and stay in NYC quite often.  My overall project architect from IBM asked me on the walk back to the IBM offices if I had a stroke. Yes, 2006, she then mentioned that she had had a stroke in 2006 also and from her physical abilities appears to have recovered much better than me.  I thought I was doing a pretty god job blending in as 'normal' but survivors can pick you out most every time.

Google Commits $20 Million to Fund Tech for People With Disabilities

If we had anything other than fucking failures of stroke associations, they would have hundreds of possibilities waiting in the wings from all the employee ideas. But we have crap.
http://www.nbcnews.com/tech/innovation/google-commits-20-million-fund-tech-peopledisabilities-n364801
Google has launched an initiative to support emerging technologies that help people with disabilities live more independently. The Google Impact Challenge: Disabilities program announced Tuesday will award up to $20 million in grants to nonprofits that work on assistive technologies. The grants will be funneled through Google's charitable arm, Google.org.
"The Google Impact Challenge: Disabilities will seek out nonprofits and help them find new solutions to some serious 'what ifs' for the disabled community," Google.org director Jacquelline Fuller said in a blog post. "We will choose the best of these ideas and help them to scale by investing in their vision, by rallying our people and by mobilizing our resources in support of their missions."
To kick things off, Google announced initial support for two organizations: a $600,000 grant to the Enable Community Foundation, which creates 3-D printed prosthetic limbs for children, and a $500,000 award to World Wide Hearing for the development of a low-cost tool kit for hearing loss using smartphone technology.

How Does a Gymnast, or Even a Fitness Walker, Keep from Falling?

When your stroke fucks up one of these systems, what is your doctor doing to recover that functionality and help you enough to prevent falling? ANYTHING AT ALL?
Mine used to be damned good, I could run across a boulder field with no problem, now I have to keep my head down and miss beautiful sights right in front of me. Damn this stroke.
How Does a Gymnast, or Even a Fitness Walker, Keep from Falling?

Tuesday, September 1, 2015

NIH grant paves way for Alzheimer's research center in Fla

If our fucking useless stroke associations wanted to do something useful for survivors they would be working on getting a similar center setup for stroke. They don't even have to be innovative, they can just follow and mimic what the Alzheimers Foundation does.
http://www.bizjournals.com/southflorida/news/2015/08/28/mount-sinai-university-of-florida-win-grant.html

5 Practical Tips from Occupational Therapists

I quit reading on the first page  when they talked about you can learn ways to compensate.
 I really expect my therapists help me recover not just compensate.
But then this is from the NSA so I don't expect anything useful from them at all. WE have to demand recovery otherwise our stroke medical professionals will never get off their asses and do the right thing.

http://www.strokesmart.org/practical-tips?page=1&id=390 
 

Most adults' 'heart age' exceeds their actual age: U.S. CDC

Mine tells me I'm 61  instead of my age of 59 but you have to lie and say you have not had a stroke to get thru the test.
Test here:
http://www.heartage.me/your-heart-age/your-health
Article here:
Most adults' 'heart age' exceeds their actual age: U.S. CDC

Share Afib awareness in September

Another failure from the National Stroke Association.

Guargantuan F*cking Whoopee.


 Who gives a shit about awareness? We want solutions/results, do that and it might be worth donating to you.
http://support.stroke.org/site/R?i=T6KxzHpdM-x6Nn9o14tHNQ

Dear Dean,
Maureen F - Sized
Watch Maureen’s story
September is Atrial Fibrillation (Afib) Awareness Month, and we are committed to bringing attention to this health condition and its connection to stroke.
Fact: Afib is a type of irregular or “racing” heartbeat that can cause blood to collect in the heart and potentially form a clot that can lead to a stroke.
Fact: Afib increases the risk for stroke by 500%.
Fact: Afib affects an estimated 2.2 million people in the U.S.
There are many stories like Maureen’s—who didn’t know she had Afib prior to having a stroke. It is estimated that one-third of patients with Afib are undiagnosed. Learn how Maureen found her voice and became her own advocate on her road to recovery.
Learn more
In health,
signed by Anna Taylor
Anna Taylor, MS
Director, Awareness and Professional Programs

Magnetic Stimulation Effective in Helping Parkinson’s Patients Walk

Would this be useful for stroke survivors? This will not be answered because we have NO stroke strategy at all and no one seems to care about that failure.
http://www.alphagalileo.org/ViewItem.aspx?ItemId=155922&CultureCode=en
Non-Invasive Treatment Shows Promise in a New Restorative Neurology and Neuroscience Report
About 50% of patients with Parkinson’s disease (PD) experience freezing of gait (FOG), an inability to move forward while walking. This can affect not only mobility but also balance. In a new study published in Restorative Neurology and Neuroscience, researchers report that repetitive transcranial magnetic stimulation (rTMS) can reduce FOG and improve other motor skills in PD patients.
In a study conducted by researchers at the Sungkyunkwan University School of Medicine, Seoul, Korea, 17 PD patients experiencing FOG were treated with either real or sham high-frequency rTMS in five sessions over a one-week period. After a two-week interval, the patients in both groups were switched to the other treatment. Patients were assessed at three times: at the beginning of the study before stimulation began (pre-rTMS at day 1), immediately after the intervention (post-rTMS at day 5), and one week after cessation of the intervention (follow up at day 12). After switching, the three assessments were repeated. All medications were kept constant throughout the study and all interventions were performed at the same time of day. Both the researchers and the patients were not informed whether real or sham treatment was being administered.
“This study demonstrated that five cumulative sessions a week of 10 Hz high-frequency rTMS was likely to alleviate FOG in patients with PD, and the effect continued for a week. Similar results were found in the motor and the gait function,” explained lead investigator Yun-Hee Kim, MD, PhD, Professor in the Department of Physical and Rehabilitation Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Republic of Korea. “This study provides evidence that the cumulative high-frequency rTMS is a good candidate as an add-on therapy for FOG in PD.”
The location in each patient’s scalp for optimal stimulation of the anterior tibialis muscle (the front of lower leg) was mapped by stimulating the muscle and moving a pickup coil over the scalp to find the greatest response. This position was then used for each treatment.
A magnetic stimulator was placed and 20 pulses of 10 Hz rTMS were delivered to the target motor cortex areas of the dominant hemisphere. Each pulse lasted five seconds, with 55-second intervals between pulses, delivering 1,000 pulses in 20 minutes. Sham stimulation was conducted with a coil held at a 90 degree position in order to ensure that the magnetic field did not stimulate the motor cortex.
Patients were evaluated after treatments using the FOG-Q, a self-assessment scale for evaluating FOG symptoms in Parkinson’s syndrome. In addition, participants were instructed to walk to a target (traffic cone) one meter behind them, turn around, and then return, as part of a Timed-Up-and-Go (TUG) task during a modified Standing-Start 180 degree Turn Test (SS-180). The TUG task was repeated twice in each direction, and the entire process was video recorded to quantify FOG.
When patients underwent real treatment, the FOG-Q and TUG at post-rTMS significantly improved compared with pre-rTMS and these results continued into the follow up period. However, there were no significant changes in FOG-Q or TUG at post-rTMS and follow-up in patients when experiencing the sham treatment.



'All stroke neurologists are worthless, they know nothing about stroke rehab. '

This meme needs to become ubiquitous.
They will protest and tell you the lie, ' All strokes are different,  all stroke recoveries are different'
To prove they know nothing, ask for documented results from previous patients,  including the stroke protocols prescribed.  If you see E.T. (evaluate and treat) that means they are relying on the spontaneous recovery in the first year, the skill of the therapists and the determination of the survivor.
Nothing in that is the skill/knowledge of the neurologist.
You're screwed unless you are smart enough to figure out your own recovery.
No one in the world has the knowledge to help you.