Use the labels in the right column to find what you want. Or you can go thru them one by one, there are only 12345 posts. Searching is done in the search box in upper left corner. I blog on anything to do with stroke.DO NOT DO ANYTHING SUGGESTED HERE AS I AM NOT MEDICALLY TRAINED, YOUR DOCTOR IS, LISTEN TO THEM. BUT I BET THEY DON'T KNOW HOW TO GET YOU 100% RECOVERED. I DON'T EITHER, BUT HAVE PLENTY OF QUESTIONS FOR YOUR DOCTOR TO ANSWER.
Deans' stroke musings
Changing stroke rehab and research worldwide now.Time is Brain!Just think of all thetrillions and trillions of neuronsthateach daybecause there areeffective 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
From the Department of Psychiatry, University of Pittsburgh School of Medicine, Pittsburgh, PA (M.J.L., R.C.T.); and Department
of Social and Behavioral Sciences, Harvard School of Public Health, Boston, MA (L.D.K.).
Correspondence to Maya J. Lambiase, PhD, Department of Psychiatry, University of Pittsburgh School of Medicine, 3811 O’Hara
St, Pittsburgh, PA 15213. E-mail MJL106@pitt.edu
Background and Purpose—Higher
levels of anxiety are associated with increased risk for coronary heart
disease. However, few studies have investigated
whether anxiety is associated with stroke
risk. The purpose of this study was to examine the association between
and incident stroke in a nationally
representative longitudinal study of the US population.
(n=6019) in the First National Health and Nutrition Examination Survey
were assessed at baseline and followed
for 16.29±4.75 years. Multivariate Cox
proportional hazards regression models were used to estimate hazard
ratios and 95%
confidence intervals of incident stroke
associated with a 1 SD increase in anxiety symptoms. Models were
adjusted for standard
cardiovascular risk factors and additionally
Results—A total of
419 incident stroke cases were identified from hospital/nursing home
discharge reports and death certificates.
Reporting more anxiety symptoms at baseline
was associated with increased risk of incident stroke after adjusting
biological and behavioral cardiovascular risk
factors (hazard ratio, 1.14; 95% confidence interval, 1.03–1.25).
when additionally controlling for depression.
Exploratory analyses considering the role of potential confounding
variables suggested that behavioral factors
may be a key pathway linking anxiety to stroke risk.
anxiety symptom levels were associated prospectively with increased risk
for incident stroke independent of other risk
factors, including depression. Anxiety is a
modifiable experience that is highly prevalent among the general
assessment and treatment may contribute to
developing more effective preventive and intervention strategies for
overall cardiovascular health.
I plan on getting there. http://www.caring.com/articles/10-clues-you-will-live-to-100
Clue #1: How many elderly relatives are on your family tree? Mostly 80s 1 90+ What it may mean: You may have longevity genes.
Clue #2: How fast and how far can you walk? I don't know What it may mean: You're in good condition for the long haul.
Faster walkers live longer. University of Pittsburgh researchers
crunched numbers from nine different studies including almost 35,000
subjects ages 65 or older. The result: For each gait speed increase of
0.1 meters per second came a corresponding 12 percent decrease in the
risk of death.
The average speed was 3 feet per second (about two miles an hour).
Those who walked slower than 2 feet per second (1.36 miles per hour) had
an increased risk of dying. Those who walked faster than 3.3 feet per
second (2.25 miles per hour) or faster survived longer than would be
predicted simply by age or gender.
A 2006 report in the Journal of the American Medical Association
found that among adults ages 70 to 79, those who couldn't walk a
quarter mile were less likely to be alive six years later. They were
also more likely to suffer illness and disability before death. An
earlier study of men ages 71 to 93 found that those who could walk two
miles a day had half the risk of heart attack of those who could walk
only a quarter mile or less.
Clue #3: Do you have a lot of people in your life? Yes What it may mean: Social engagement is a key lifespan-extender.
Clue #4: Are you a woman? No What it may mean: Odds are more in your favor from the start.
Clue #5 (for women only): Did you have a child after age 35? What it may mean: This is possible evidence that you're a slow ager.
Clue #6: When were you born? What it may mean: Growing lifespans give younger people an edge.
And if you're 99 now? You have a whopping 67 percent chance of seeing another year.
Clue #7: Do you worry -- but not too much? NO What it may mean: There's a "healthy" worry level.
Clue #8: Is your weight normal -- or are you only slightly overweight? Yes What it may mean: You have better odds of reaching 100 than if you were obese.
A surprising 2011 Albert Einstein College of Medicine study of 477
adults ages 95 to 112 found that these solid-gold agers had no better
health habits overall than a comparison group born at the same time that
had been studied in the 1970s. One difference: Those in long-lived
group were much less likely to be obese.
Both male and female centenarians in the study were overweight at
about the same rates as those in the shorter-lived group. But only 4.5
percent of the long-lived men and 9.6 of the women were obese, compared
to 12.1 percent and 16.2 percent, respectively, of the younger-lived
controls. ("Normal weight" is a Body Mass Index -- or BMI, a measure of
height in proportion to weight -- in the range of 18 to 24; "overweight"
is 25 to 30; over 30 is "obese.")
This finding echoes other studies showing the greatest risks of death
among those who are obese or underweight at age 65 (BMI under 18.5),
compared to those of normal weight or slight overweight. A 2011 study at
Loma Linda University in Southern California found that men over age 75
with a BMI over 27.4 lived nearly four years less than those with a
lower BMI. For women over age 75, a BMI over 27.4 led to a two-year
shorter lifespan. Studies of centenarians show that men who reach 100
are almost always lean (more so than women).
Luckily, this clue is one you can control. "Since you can't be sure
if you'll live to 100, I wouldn't take the chance of ignoring the
lifestyle interventions that we know will at least put you in the half
the population who die after age 80 -- starting with watching weight and
being sure to exercise," says the senior author of the Albert Einstein
study, Nir Barzilai, director of the college's Institute for Aging
Clue # 9: How long are your telomeres? Who knows? There's this:
What it may mean: Many people who live to 100 have a hyperactive version of an enzyme that rebuilds telomeres.
Clue #10: Are you a positive person? Yes What it may mean: Emotion influences health, which influences aging. But what about the research that says that pessimists live longer?
Few medical conditions, neurological or otherwise, exact a greater public-health toll than stroke, a fact underscored by a new published report
on the global burden of stroke. An acute brain injury that may begin
insidiously years prior, stroke is now the second leading cause of death
and the third most common cause of disability worldwide. Nearly 17
million people in the world will have a first stroke in the next year,
and 33 million people are stroke survivors.
In the U.S., stroke is
the No. 1 cause of serious long-term disability. Approximately 800,000
strokes occur annually in this country, and about 130,000 people die
annually from stroke. The risk of stroke has decreased by roughly 70
percent in the U.S. since incidence was first tracked in the mid-1900’s,
a downward trend that has not plateaued, suggesting there is still room
for improvement. Stroke risk factors are well known, and experts
estimate that 80 percent of strokes could be prevented with better
management of hypertension, blood lipids, and glucose. Getting Aggressive About Prevention
people believe there could be substantial, dramatic stroke reduction if
we just really aggressively managed the risk factors we currently know
about,” says Walter Koroshetz, M.D., deputy director of the National
Institute for Neurological Disorders and Stroke and a member of the Dana
Alliance for Brain Initiatives. “In many diseases, you need a major
scientific breakthrough to make a difference. That’s not true with
stroke.” Except you could reduce stroke risk by hundreds of percents following these;
Green tea and coffee 20% - Green tea, coffee may reduce stroke risk by 20 percent
Opening the Window for Acute Treatment
advocates have tried for years to drive home the message that strokes
require immediate medical attention, ever since a treatment became
available that could help some people with ischemic stroke, which occurs
when blood flow to part of the brain is restricted by a clot or
narrowed blood vessel. Tissue plasminogen activator, or tPA, is still
the only drug approved for treating acute stroke, but its use is
severely limited, largely because published guidelines call for it to be
administered within three hours of stroke onset for most patients. Some
experts have criticized these guidelines and are calling for them to be
revised. With a pathetic 12% efficacy that means that they are lying about 88% of the results
Public Awareness Still Lacking
advent of tPA has triggered a system-wide reorganization of stroke
urgent care that is still evolving nearly 17 years later. For example,
specialized stroke centers have been established where expert care,
along with the tools and technologies for swift, accurate diagnosis, is
readily available. A tiered system based on minimum requirements, much
like the system that designates hospitals as Level 1-4 trauma centers
depending on their capabilities, is being put in place for stroke care
as well, so that patients can be transported to the most advanced center
in their area. While there have been vast improvements, a number of
obstacles remain. Primary among them is public awareness, experts say.
knowledge about stroke is still very low,” says Caplan. “This is the
more difficult problem, because a lot of people don’t know they’ve had a
stroke.” The real problem here is that there is no easy objective way to diagnose a stroke. Friends have been in ERs for hours because the stroke hadn't established severe enough effects to be obvious. That should be accomplished with the tricorder possibly thru one of these 17 ways. Better Rehab Through Brain Science
Global Burden of Disease report underscores the dichotomy between
richer, developed countries like the U.S., where the majority of people
who suffer a stroke survive, and poorer, developing countries where
people are more likely to die from a stroke. While cutting stroke deaths
is a major global-health goal, better recovery and rehabilitation
strategies are desperately needed to address the ever-growing population
of stroke survivors who struggle to function with varying degrees of
“We have in the U.S. alone 800,000 people who have a
stroke each year. So the question becomes, what can be done to return
functional recovery to those patients?” says Koroshetz. “That’s where
the really interesting science is, because it intersects with the area
of neuroplasticity–how the brain learns to function for a particular
purpose and how it rewires itself to get lost function back.” You have this all wrong, you need to stop the neuronal cascade of death resulting in much less death and disability. The silo of rehabilitation is not where the breakthroughs are going to occur because no one knows exactly how to make neuroplasticity repeatable. Brain Recovery Not Passive
Armed with such
investigational tools, neuroscience has already revealed some
fundamental principles of recovery in the brain. “The general rule, at
least in the cortex, is that somehow the brain recovers function after
an initial injury, whether it’s a stroke or some other lesion,” says
Koroshetz. “Now people are studying how that happens, and the hope is
that we can translate that to therapeutic strategies.”
finding already, Koroshetz says, is that recovery from injury is not
“passive.” Rather, it requires enhancement by active exposure to sensory
stimuli or motor practice. He points to the LEAPS study,
which was the first large randomized, controlled clinical trial that
investigated recovery of locomotor function in people who had had a
stroke. The NIH-funded study compared two fairly intensive therapies:
treadmill walking vs. strength and balance training performed at home
with a physical therapist. A third group, serving as controls, received
“standard of care”–whatever physical therapy or rehab they were getting
as part of their regular medical care. ‘Standard of Care’ Substandard? What the hell is the standard of care for stroke? Does anyone know?
“What have you done to make your dream come true?”
I was scared that I wouldn’t be good enough, posh enough, young enough, confident enough, and Lord-knows-what-else enough to learn how to play a musical instrument.
I hate the way my walking looks, my hip hikes, my foot swings out, my knee barely bends. The only thing that mostly recovered is I can dorsiflex the foot by thinking about it. But I'll walk every weekend in the trails in the woods, falling down doesn't occur too much anymore. And my skiing is atrocious, it would be even worse if I had to step over all the fallen limbs and trees I cleared in the past 4 months. Right now I'd call it shuffling on skis, there is no glide yet.
Too many of my email correspondents want the instant rehab - if only I can find the right therapy/therapist.
I think the best advice our doctors and therapists could give us would be; There are NO shortcuts to stroke rehab, its going to look ugly for a long time. We have no idea how much you'll recover. Are YOU willing to put in the time and effort to recover?
A long time ago in my job in technology we had a technical help desk for when programmers were stumped. They were helped by the analyst answering the phone or directed to the expert in the area. I once was perplexed by a difficult problem and called the help desk. The analyst didn't know the answer and after finding out I was supporting the life insurance area, directed me to Dean R. I was asked if I knew that person. Yeah, thats me. Recovering from stroke feels exactly the same way, there is no more knowledgeable person I can go to for answers. You could try the ASA- American Stroke Association helpline 1-888-4-STROKE but I'm sure that won't do a damn bit of good.
Or the NSA - National Stroke Association 1-800-STROKES (787-6537)
The WSO - World Stroke Organization has no numbers for survivors to contact them because they are not for survivors.
Or maybe the uk Stroke Helpline: 0303 3033 100 Or maybe The Stroke Organization at the End of the Universe -1-800-youarescrewed
The effect of simvastatin on Wnt is through inhibited prenylation
improve recovery from traumatic brain injury and show promise in
preventing Alzheimer disease. However, the mechanisms by which statins
may be therapeutic for neurological conditions are not fully understood.
In this study, we present the initial evidence that oral administration
of simvastatin in mice enhances Wnt signaling in vivo. Concomitantly,
simvastatin enhances neurogenesis in cultured adult neural progenitor
cells as well as in the dentate gyrus of adult mice. Finally, we find
that statins enhance Wnt signaling through regulation of isoprenoid
synthesis and not through cholesterol. These findings provide direct
evidence that Wnt signaling is enhanced in vivo by simvastatin and that
this elevation of Wnt signaling is required for the neurogenic effects
of simvastatin. Collectively, these data add to the growing body of
evidence that statins may have therapeutic value for treating certain
Environmental Enrichment (EE) is shown to facilitate recovery of motor
and cognitive function in animal models of stroke. The efficacy of EE in
the clinical setting with stroke survivors remains unknown. Successful
implementation of EE in a busy rehabilitation unit requires
identification of barriers and enablers which are best informed by staff
feedback. Aim: To qualitatively explore the experiences of
nursing staff involved in a pilot study investigating the feasibility of
EE in a rehabilitation ward. Methods: This was a qualitative
study consisting of analysis of semi-structured interviews with nine
nursing staff who were asked to reflect on “routine care” and their own
“experience of the EE study”. An inductive thematic approach was used to
collect and analyse data using a process of constant comparison. Results:
Male and female staff with varying years of experience working in
stroke rehabilitation participated in focus group and individual
interviews. Three key themes were identified concerning the
implementation of EE including: (i) “Nurses are so busy” – perceptions
on routine work practice; (ii) “A better outlook” – perceptions of the
benefit of EE; (iii) “They’re just not going to participate” –
perceptions of barriers to EE. Indeed, the challenges identified in this
study align with practice change literature, which indicates that staff
workload, routine and attitudes can influence the implementation of a
new practice. Discussion: Staff perceived the use of an EE in
their rehabilitation unit promoted activity/participation and increased
patient moral. The barriers and enablers experienced by staff in this
study may be used to inform the design and conduct of future studies
investigating the efficacy of EE during inpatient stroke rehabilitation
purposes of this study were to examine the current Brain Trauma
Foundation recommendation for antiseizure prophylaxis with phenytoin
during the first 7 days after traumatic brain injury (TBI) in preventing
seizures and to determine if this medication affects functional
recovery at discharge.
The records of adult (age
≥ 18 years) patients with blunt severe TBI who remained in the hospital
at least 7 days after injury were retrospectively reviewed from January
2008 to January 2010. Clinical seizure rates during the first 7 days
after injury and functional outcome at discharge were compared for the
two groups based on antiseizure prophylaxis, no prophylaxis (NP) versus
phenytoin prophylaxis (PP). Statistical analysis was performed using χ.
total of 93 adult patients who met the previously mentioned criteria
were identified (43 [46%] NP group vs. 50 [54%] PP group). The two
groups were well matched. Contrary to expectation, more seizures
occurred in the PP group as compared with the NP group; however, this
did not reach significance (PP vs. NP, 2 [4%] vs. 1 [2.3%], p = 1).
There was no significant difference in the two groups (PP vs. NP) as far
as disposition are concerned, mortality caused by head injury (4 [8%]
vs. 3 [7%], p = 1), discharge home (16 [32%] vs. 17 [40%], p = 0.7), and
discharge to rehabilitation (30 [60%] vs. 23 [53%], p = 0.9). However,
with PP, there was a significantly longer hospital stay (PP vs. NP, 36
vs. 25 days, p = 0.04) and significantly worse functional outcome at
discharge based on Glasgow Outcome Scale (GOS) score (PP vs. NP, 2.9 vs.
3.4, p < 0.01) and modified Rankin Scale score (2.3 ± 1.7 vs. 3.1 ±
1.5, p = 0.02).
PP may not decrease early
posttraumatic seizure and may suppress functional outcome after blunt
TBI. These results need to be verified with randomized studies before
recommending changes in clinical practice and do not apply to
And since we already can grow brains on a chip this style of testing might solve rodent model in inflammation is not the same as humans. At least that could be the case if we had a great stroke association directing where research should be going. http://news.ubc.ca/2013/12/30/organs-on-a-chip-2/
if medical research and clinical drug tests could be done on
artificially grown organs on microchips to save time, costs, and ease
That’s the dream of James Feng, a professor in biological and chemical engineering at UBC.
“The potential is tremendous,” says Feng. “The main impact of organs
grown this way will be on the design of drugs; the understanding of the
Dr. Feng’s group carries out research in three broad areas: mechanics
of biological cells and tissues, interfacial fluid dynamics,
and mechanics and rheology of complex fluids.
The group has an inter-disciplinary flavour–crosscutting applied
mathematics, cell biology, soft-matter physics and chemical and
biomedical engineering—that is well-suited for exploring this burgeoning
technology. Implications for the pharmaceutical industry
Feng cites a Harvard study
using a small silicon device that holds a thin layer of real cell
membranes capable of producing motion similar to the heaving and
breathing of a lung.
Organ models designed this way have the potential to be more accurate
in drug and treatment trials, says Feng, as they can better mimic the
functions of human organs, as opposed to animal models which are the
current research standard.
“It’s more controlled and you can simplify the process much faster,” said Feng.
“Harvard researchers also injected drugs into their chip model to see
how it changed its behaviour and to see the tissue’s reaction to
mechanical or chemical disturbance,” he added.
“It’s very important for drug design and discovery and the pharmaceutical industry would be tremendously interested in that.”
In addition, organs on a chip present a less controversial option for
organ model testing compared to stem cell research. According to Feng,
this is because their ultimate goals are very different from each other.
“The research that tried to grow organs directly from stem cells is
aiming for eventually implantable organs,” he said. “The idea of making
the chip is to work toward replacing animal models, so as to be more
accurate and realistic like human organs. While the ability to replicate
a complex human organ function remains far off, the direction appeals
to anyone who is hoping to reduce the use of animals in research.” Simulating organ functions on a chip
Feng says this kind of organ testing offers the possibility of greatly reducing cost and time required for clinical trials.
“By using computer simulations we can generate results and insights,
and run virtual tests much more easily and quickly,” he says.
“We can test maybe hundreds or thousands of designs of organ chips to
be able to tell you whether you should try those ten designs instead of
the hundreds one by one.”
Feng, who has a background in aerospace engineering, says this new
bio-technology has the potential to transform the development of
artificial organs and drugs the way computer simulations have replaced
the use of wind tunnels for designing aircrafts.
“That used to be the dominant mode of designing crafts,” he said,
“but that’s being replaced by online computer simulations because we
understand the principles of aerodynamics so well.”
While UBC’s efforts in the field are in the early stages, Feng is
reaching out to researchers from other backgrounds. He will be inviting
leading scientists to UBC in July 2014 for a workshop that will centre
on the growth of artificial organs and computer simulations. He is also
exploring ideas of his own.
“I have a collaboration with an engineering colleague on how to use
the microfluidic chip, the technology used to emulate the lung in the
Harvard study, as a way of measuring malaria-infected red cells,” he
said, suggesting that this is just one of the countless ways this new
technology could be used to fuel future innovation.
I'm sure your doctor is not using this to determine the effectiveness of stroke interventions. As of 2003 there seems to be no use of it for stroke survivors. Unless our worthless stroke associations have done something since I bet no one cares about our Quality of Life. In fact its probably better if you just die, my ex-wife would have preferred that. http://www.hqlo.com/content/1/1/60
The Quality of Life Scale (QOLS), created originally by American psychologist John
Flanagan in the 1970's, has been adapted for use in chronic illness groups. This paper
reviews the development and psychometric testing of the QOLS. A descriptive review
of the published literature was undertaken and findings summarized in the frequently
asked questions format. Reliability, content and construct validity testing has been
performed on the QOLS and a number of translations have been made. The QOLS has low
to moderate correlations with physical health status and disease measures. However,
content validity analysis indicates that the instrument measures domains that diverse
patient groups with chronic illness define as quality of life. The QOLS is a valid
instrument for measuring quality of life across patient groups and cultures and is
conceptually distinct from health status or other causal indicators of quality of
Quality of Life Scale; QOLS; chronic illness outcomes; quality of life evaluation
Why assess Quality of Life in chronic illness?
Quality of life (QOL) measures have become a vital and often required part of health
outcomes appraisal. For populations with chronic disease, measurement of QOL provides
a meaningful way to determine the impact of health care when cure is not possible.
Over the past 20 years, hundreds of instruments have been developed that purport to
measure QOL . With few exceptions, these instruments measure what Fayers and colleagues [2,3] have called causal indicators of QOL rather than QOL itself. Health care professionals
need to be clear about the conceptual definition of QOL and not to confound it with
functional status, symptoms, disease processes, or treatment side-effects [4-7]. Although the definition of QOL is still evolving, Revicki and colleagues define
QOL as "a broad range of human experiences related to one's overall well-being. It
implies value based on subjective functioning in comparison with personal expectations
and is defined by subjective experiences, states and perceptions. Quality of life,
by its very natures, is idiosyncratic to the individual, but intuitively meaningful
and understandable to most people [, p. 888]." This definition denotes a meaning for QOL that transcends health. The
Quality of Life Scale (QOLS) first developed by American psychologist, John Flanagan,
[9,10] befits this definition of QOL.
And rather than looking for other preventive ideas, they go down the failed route of telling us generalities like control hypertension, eat better. Like this worthless statement - The association encourages patients to change their lifestyle to
decrease their risk of stroke and to treat their medical risks by
working with their doctors. http://atlantablackstar.com/2013/12/28/southern-united-states-also-known-stroke-belt/
Maybe you want to ask your doctor about these 10 prevention ideas. But they come from me, a non-medical person, so they are automatically worthless.
Researchers at The University of Texas at Dallas have taken a step
toward developing a new treatment to aid the recovery of limb function
In a study published online in the journal Neurobiology of Disease, researchers report the full recovery of forelimb strength in animals receiving vagus nerve stimulation.
“Stroke is a leading cause of disability worldwide,” said Dr. Navid
Khodaparast, a postdoctoral researcher in the School of Behavioral and
Brain Sciences and lead author of the study. “Every 40 seconds, someone
in the U.S. has a stroke. Our results mark a major step in the
development of a possible treatment.”
Vagus nerve stimulation (VNS) is an FDA-approved method for treating
various illnesses, such as depression and epilepsy. It involves sending a
mild electric pulse through the vagus nerve, which relays information
about the state of the body to the brain.
Khodaparast and his colleagues used vagus nerve stimulation precisely
timed to coincide with rehabilitative movements in rats. Each of the
animals had previously experienced a stroke that impaired their ability
to pull a handle.
Stimulation of the vagus nerve causes the release of chemicals in the
brain known to enhance learning and memory called neurotransmitters,
specifically acetylcholine and norepinephrine. Pairing this stimulation
with rehabilitative training allowed Khodaparast and colleagues to
A biased writeup in favor of homeopathy here;
It has the standard excuse that traditional scientific methods can't be used because they don't honor the principles of homeopathy. What a load of crock. They have to disparage the scientific method because that method proves that homeopathy is nothing more than placebo. So if you are going down this route ask for scientific research, not this type of misleading puff piece.
Fascinating ideas from this one, a couple of lines for your amusement.
There are following remedies which are helpful in the treatment of cerebral stroke: Aconite Nap.: good remedy for stroke, for a person who is panicky and fear of dying. Aurum mur: when stroke is caused by depression or while person loses his face. Opium: excellent remedy for apoplexy; comma and
obstructed respiration; patient lies down; loss of consciousness with
eyes half open after the brain hemorrhage. And where the hell is this person going to get opium? Never mind, after succussing numerous times there is no actual atoms of the original element in the result, so there is no need to even start out with the named element. Unless you happen to believe in magical water memory.
And absolutely no mention of doing anything to stop the neuronal cascade of death. Solve that and you can congratulate yourself, until then you have very little to be pleased about. http://www.medpagetoday.com/Cardiology/Strokes/39440?
Stroke care networks save lives and reduce the need for long-term
care, a study of one of the largest and longest operating networks
In an integrated system of stroke care delivery in
Ontario mortality rates 30 days after hemorrhagic stroke decreased from
38.3% to 34.4% after the networks were fully implemented (P<0.001) and discharge to a long-term care or chronic care facility dropped from 16.9% to 14.8% (P<0.001),
reported Moira Kapral, MD, of the University of Toronto Institute for
Clinical Evaluative Sciences, and colleagues in CMAJ.
10-year study included data on 243,287 patient visits to emergency
departments (ED) and 163,198 hospital admissions for acute stroke or
transient ischemic attack before and after 2005, when the stroke care
network became fully operational in Ontario.
are designed to integrate the delivery of stroke treatment across
regions to optimize the chances that patients will receive timely,
evidence-based therapies even if they don't live near a designated
"After the stroke network was introduced there were clear improvements in the quality of stroke care," Kapral told MedPage Today.
"More patients were treated with optimal stroke care interventions,
such as thrombolysis, including clot-busting drugs, and stroke-unit
Kapral's group used population-based provincial
administrative databases to identify all ED visits and hospital
admissions for acute stroke and transient ischemic attack from 2001 to
They assessed the effect of the full implementation of the
Ontario Stroke System in 2005 on the proportion of patients who received
care at stroke centers, and on rates of discharge to long-term care
facilities and 30-day mortality after stroke.
The proportion of
patients who received care at either a regional or district stroke
center increased from 40% before 2005 to 46.5% after full implementation
of the system (P<0.001). The median time from stroke presentation to carotid revascularization decreased from 50 to 22 days (P<0 .001="" p="">Piecewise
regression analysis showed a gradual increase in the rate of care at
stroke centers before 2005, followed by a significant upward shift in
rates in 2005.
And significant increases were seen between 2002 and 2009 in rates for the following (P<0.001 for all):
Thrombolytic therapy use: 10% to 27%
Neuroimaging: 77% to 93%
Carotid imaging: 44% to 68%
Care in a stroke unit: 3% to 24%
Dysphagia screening: 47% to 57%
Antithrombotic therapy: 80% to 94%
far the biggest improvements were seen at regional and district stroke
centers, with little or no change evident at nondesignated centers, the
The authors cautioned that "although we observed
an increase in the proportion of patients seen at designated stroke
centers over the study period, the absolute magnitude of the increase
was modest, with more than half of the population receiving care at
nondesignated centers even 5 years following the full implementation of
the stroke system."
They suggested that this was the result of the
system being designed mostly to facilitate the transfer, or bypass, of
those patients most likely to be good candidates for thrombolytic
therapy or neurosurgical interventions.
Nonetheless, the decreases
would be expected to result in about 200 fewer stroke-related deaths
and 300 fewer patients requiring long-term care or chronic care
annually, they pointed out.
The researchers conceded that
significant regional variations in care persist, and they acknowledged
that Ontario's large and geographically diverse territory has made the
implementation of an integrated stroke care network a challenge.
said increased utilization of telemedicine and other efforts to provide
evidence-based therapies to patients not treated at designated stroke
centers should improve patient outcomes.
The Ontario Telestroke
Program has provided neurologist consultations for stroke patients
treated at regional hospitals without stroke centers over the last
decade and 30% received thrombolytic treatments.
"Despite our best
efforts, there will always be patients who just don't live close enough
to a stroke center to be treated at one," she said. "That is why
networks are especially important in rural and remote areas."
study had some limitations. The authors focused on hospital-based
processes of care and outcomes and did not have data on longer-term
outcomes such as functional status, quality of life, or after-stroke
care. Also, the piecewise regression analyses did not account for the
potential effects of concurrent interventions.
concluded that the findings provide stroke support for the ongoing
development and implementation of networks to coordinate the delivery of
stroke care, and that "future research should focus on identifying the
specific components of such systems that are most likely to account for
improvements in outcomes."
I would think if we had any smart doctors or hospital administrators they would be using this to make sure the meals in the hospital post-stroke were cognitive friendly. Unless you are on Warfarin and need to stay away from vitamin K.
But I can almost 100% guarantee that absolutely nothing will be done to help your stroke recovery in this regard. Because we have shit for stroke associations and lead-assed inertia for doctors and stroke centers.
But thats just my reasoned opinion, if you have some proof otherwise please respond. http://www.neurobiologyofaging.org/article/S0197-4580%2813%2900244-3/abstract
is accumulating that vitamin K could have a role in cognition,
especially in aging. Using data from the Québec Longitudinal Study on
Nutrition and Successful Aging (NuAge), a cross-sectional analysis was
conducted to examine the associations between vitamin K status, measured
as serum phylloquinone concentrations, and performance in verbal and
non-verbal episodic memory, executive functions, and speed of
processing. The sample included 320 men and women aged 70 to 85 years
who were free of cognitive impairment. After adjustment for covariates,
higher serum phylloquinone concentration (log-transformed) was
associated with better verbal episodic memory performances (F = 2.43, p = 0.048); specifically with the scores (Z-transformed)
on the second (β = 0.47; 95% confidence interval [CI] = 0.13–0.82),
third (β = 0.41; 95% CI = 0.06–0.75), and 20-minute delayed (β = 0.47;
95% CI = 0.12–0.82) free recall trials of the RL/RI-16 Free and Cued
Recall Task. No associations were found with non-verbal episodic memory,
executive functions, and speed of processing. Our study adds evidence
to the possible role of vitamin K in cognition during aging,
specifically in the consolidation of the memory trace.
neurons were discovered over twenty years ago in the ventral premotor
region F5 of the macaque monkey. Since their discovery much has been
written about these neurons, both in the scientific literature and in
the popular press. They have been proposed to be the neuronal substrate
underlying a vast array of different functions. Indeed so much has been
written about mirror neurons that last year they were referred to,
rightly or wrongly, as “The most hyped concept in neuroscience”. Here we
try to cut through some of this hyperbole and review what is currently
known (and not known) about mirror neurons.
Critics of the power of positive thinking often say it is a naive world
view that refuses to look at the facts. "Life is hard and then you die"
is their motto. Psychologists and others who have studied the subject in
depth disagree. Truly positive thinkers, far from hiding their heads in
the sand, face life's challenges head-on because they are able to learn
and grow from negative experiences and take advantage of existing
She obviously learned from her previous failures. Are you learning from all the hundreds of thousands of failures you will need to experience to recover?
Found this empty bottle in the parking lot after clearing the inner loop of the trail in two hours. It was wonderful, 50 degrees out and I'll be able to at least ski one loop this winter. Only 2 falls into the wet snow and getting up is an exercise in getting every inch of your pants wet.
Imitation Chocolate Chip Cookie Dough Flavored Vodka, the smell is not great. As compared to the Johnnie Walker Blue Label I had last night.