Use the labels in the right column to find what you want. Or you can go thru them one by one, there are only 29,286 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.
Changing stroke rehab and research worldwide now.Time is Brain!trillions and trillions of neuronsthatDIEeach day because there areNOeffective 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.
The term Charcot–Wilbrand syndrome
(CWS) denotes dream loss following focal brain damage. We report the
first case of CWS, in whom neuropsychological functions, extension of
the underlying lesion, and sleep architecture changes were assessed. A
73-year-old woman reported a total dream loss after acute, bilateral
occipital artery infarction (including the right inferior lingual
gyrus), which lasted for over 3 months. In the absence of sleep–wake
complaints and (other) neuropsychological deficits, polysomnography
demonstrated an essentially normal sleep architecture with preservation
of REM sleep. Dreaming was denied also after repeated awakenings from
REM sleep. This observation suggests that CWS (1) can represent a
distinct and isolated neuropsychological manifestation of deep occipital
lobe damage, and (2) may occur in the absence of detectable REM sleep
abnormalities. Ann Neurol 2004
Nothing to do with stroke. On Sunday in order to get my 70,000 steps for the week I needed 13,000 steps due to social activities on Friday and Saturday, wine was included. Saw this scat on the trail, looks to me like mouse hairs in there but no clue what animal would have produced this, size is 1.25-1.5 inches in diameter. Many pools of water were waded thru with my Wellies, zero snow on the ground
Just in rats so YOU will need to ask your doctor what research group they are collaborating with to test this in humans. No collaboration, call the hospital president and demand the incompetent stroke department head be fired. Someone has to light a fire under our stroke medical professionals since they aren't doing it themselves. Yes, I am a bad person, wanting some competency in stroke recovery. http://stroke.ahajournals.org/content/early/2017/02/23/STROKEAHA.116.015204
Hongqi Xin, Mark Katakowski, Fengjie Wang, Jian-Yong Qian, Xian Shuang Liu, Meser M. Ali, Benjamin Buller, Zheng Gang Zhang, Michael Chopp
Background and Purpose—Multipotent
mesenchymal stromal cell (MSC) harvested exosomes are hypothesized as
the major paracrine effectors of MSCs. In vitro, the miR-17–92 cluster
promotes oligodendrogenesis, neurogenesis, and axonal outgrowth. We,
therefore, investigated whether the miR-17–92 cluster–enriched exosomes
harvested from MSCs transfected with an miR-17–92 cluster plasmid
enhance neurological recovery compared with control MSC-derived
exosomes.
Methods—Rats
subjected to 2 hours of transient middle cerebral artery occlusion were
intravenously administered miR-17–92 cluster–enriched exosomes, control
MSC exosomes, or liposomes and were euthanized 28 days post–middle
cerebral artery occlusion. Histochemistry, immunohistochemistry, and
Golgi–Cox staining were used to assess dendritic, axonal, synaptic, and
myelin remodeling. Expression of phosphatase and tensin homolog and
activation of its downstream proteins, protein kinase B, mechanistic
target of rapamycin, and glycogen synthase kinase 3β in the peri-infarct
region were measured by means of Western blots.
Results—Compared
with the liposome treatment, both exosome treatment groups exhibited
significant improvement of functional recovery, but miR-17–92
cluster–enriched exosome treatment had significantly more robust effects
on improvement of neurological function and enhancements of
oligodendrogenesis, neurogenesis, and neurite remodeling/neuronal
dendrite plasticity in the ischemic boundary zone (IBZ) than the control
MSC exosome treatment. Moreover, miR-17–92 cluster–enriched exosome
treatment substantially inhibited phosphatase and tensin homolog, a
validated miR-17–92 cluster target gene, and subsequently increased the
phosphorylation of phosphatase and tensin homolog downstream proteins,
protein kinase B, mechanistic target of rapamycin, and glycogen synthase
kinase 3β compared with control MSC exosome treatment.
Conclusions—Our
data suggest that treatment of stroke with tailored exosomes enriched
with the miR-17–92 cluster increases neural plasticity and functional
recovery after stroke, possibly via targeting phosphatase and tensin
homolog to activate the PI3K/protein kinase B/mechanistic target of
rapamycin/glycogen synthase kinase 3β signaling pathway.
It’s a good time to be interested in the brain. Neuroscientists can now turn neurons on or off with just a flash of light, allowing them to manipulate the behavior of animals with exceptional precision. They can turn brains transparent and seed them with glowing molecules to divine their structure. They can record the activity of huge numbers of neurons at once. And those are just the tools that currently exist. In 2013, Barack Obama launched the Brain Research through Advancing Innovative Neurotechnologies (BRAIN) Initiative—a $115 million plan to develop even better technologies for understanding the enigmatic gray blobs that sit inside our skulls. John Krakaeur,
a neuroscientist at Johns Hopkins Hospital, has been asked to BRAIN
Initiative meetings before, and describes it like “Maleficent being
invited to Sleeping Beauty’s birthday.” That’s because he and four
like-minded friends have become increasingly disenchanted by their
colleagues’ obsession with their toys. And in a new paper
that’s part philosophical treatise and part shot across the bow, they
argue that this technological fetish is leading the field astray.
“People think technology + big data + machine learning = science,” says
Krakauer. “And it’s not.” He and his fellow curmudgeons argue that brains are special because of the behavior
they create—everything from a predator’s pounce to a baby’s cry. But
the study of such behavior is being de-prioritized, or studied “almost
as an afterthought.” Instead, neuroscientists have been focusing on
using their new tools to study individual neurons, or networks of
neurons. According to Krakauer, the unspoken assumption is that if we
collect enough data about the parts, the workings of the whole will
become clear. If we fully understand the molecules that dance across a
synapse, or the electrical pulses that zoom along a neuron, or the web
of connections formed by many neurons, we will eventually solve the
mysteries of learning, memory, emotion, and more. “The fallacy is that
more of the same kind of work in the infinitely postponed future will
transform into knowing why that mother’s crying or why I’m feeling this
way,” says Krakauer. And, as he and his colleagues argue, it will not.
That’s because behavior is an emergent
property—it arises from large groups of neurons working together, and
isn’t apparent from studying any single one. You can draw parallels with
the flocking of birds. Biologists have long wondered how they manage to
wheel about the skies in perfect coordination, as if they were a single
entity. In the 1980s, computer scientists showed that this can happen
if each bird obeys a few simple rules, which dictate their distance and
alignment relative to their peers. From these simple individual rules,
collective complexity emerges.But
you would never have been able to predict the latter from the former.
No matter how thoroughly you understood the physics of feathers, you
could never have predicted a murmuration of starlings
without first seeing it happen. So it is with the brain. As British
neuroscientist David Marr wrote in 1982, “trying to understand
perception by understanding neurons is like trying to understand a
bird’s flight by studying only feathers. It just cannot be done.” A landmark study, published last year, beautifully illustrated his point using, of all things, retro video games. Eric Jonas and Konrad Kording examined the MOS 6502 microchip, which ran classics like Donkey Kong and Space Invaders,
in the style of neuroscientists. Using the approaches that are common
to brain science, they wondered if they could rediscover what they
already knew about the chip—how its transistors and logic gates process
information, and how they run simple games. And they utterly failed.
“What
we extracted was so incredibly superficial,” Jonas told me last year.
And “in the real world, this would be a millions-of-dollars data set.”
If the kind of neuroscience that has come to dominate the field couldn’t
explain the workings of a simple, dated microchip, how could it hope to
explain the brain—reputedly the most complex object in the universe?
The solution to finding out exactly how neuroplasticity works is right here. What signals is a neuron sending to a neighbor to get it to drop its current functionality and take on new functionality? If we had ANY stroke leadership and strategy we could submit an RFP to researchers to figure this out and make a protocol out if it. Thus short cutting the process of neuroplasticity by months or years and millions of repetitions.
Which research team is your stroke hospital working with? Not working with any is pure incompetency.
But this will never occur since we have fucking failures of stroke associations. https://www.sciencedaily.com/releases/2017/02/170222145750.htm
Three-in-one design allows genetic, chemical, optical, and electrical inputs and outputs.
Date:
February 22, 2017
Source:
Massachusetts Institute of Technology
Summary:
For the first time, a single multifunction
flexible fiber no bigger than a human hair, has successfully delivered a
combination of optical, electrical and chemical signals back and forth
into the brain.
For the first time ever, a single flexible
fiber no bigger than a human hair has successfully delivered a
combination of optical, electrical, and chemical signals back and forth
into the brain, putting into practice an idea first proposed two years
ago. With some tweaking to further improve its biocompatibility, the new
approach could provide a dramatically improved way to learn about the
functions and interconnections of different brain regions.
The new fibers were developed through a collaboration among material
scientists, chemists, biologists, and other specialists. The results are
reported in the journal Nature Neuroscience, in a paper by
Seongjun Park, an MIT graduate student; Polina Anikeeva, the Class of
1942 Career Development Professor in the Department of Materials Science
and Engineering; Yoel Fink, a professor in the departments of Materials
Science and Engineering, and Electrical Engineering and Computer
Science; Gloria Choi, the Samuel A. Goldblith Career Development
Professor in the Department of Brain and Cognitive Sciences, and 10
others at MIT and elsewhere.
The fibers are designed to mimic the softness and flexibility of
brain tissue. This could make it possible to leave implants in place and
have them retain their functions over much longer periods than is
currently possible with typical stiff, metallic fibers, thus enabling
much more extensive data collection. For example, in tests with lab
mice, the researchers were able to inject viral vectors that carried
genes called opsins, which sensitize neurons to light, through one of
two fluid channels in the fiber. They waited for the opsins to take
effect, then sent a pulse of light through the optical waveguide in the
center, and recorded the resulting neuronal activity, using six
electrodes to pinpoint specific reactions. All fof this was done through
a single flexible fiber just 200 micrometers across -- comparable to
the width of a human hair.
Previous research efforts in neuroscience have generally relied on
separate devices: needles to inject viral vectors for optogenetics,
optical fibers for light delivery, and arrays of electrodes for
recording, adding a great deal of complication and the need for tricky
alignments among the different devices. Getting that alignment right in
practice was "somewhat probabilistic," Anikeeva says. "We said, wouldn't
it be nice if we had a device that could just do it all."
After years of effort, that's what the team has now successfully
demonstrated. "It can deliver the virus [containing the opsins] straight
to the cell, and then stimulate the response and record the activity --
and [the fiber] is sufficiently small and biocompatible so it can be
kept in for a long time," Anikeeva says.
Since each fiber is so small, "potentially, we could use many of them
to observe different regions of activity," she says. In their initial
tests, the researchers placed probes in two different brain regions at
once, varying which regions they used from one experiment to the next,
and measuring how long it took for responses to travel between them.
The key ingredient that made this multifunctional fiber possible was
the development of conductive "wires" that maintained the needed
flexibility while also carrying electrical signals well. After much
work, the team was able to engineer a composite of conductive
polyethylene doped with graphite flakes. The polyethylene was initially
formed into layers, sprinkled with graphite flakes, then compressed;
then another pair of layers was added and compressed, and then another,
and so on. A member of the team, Benjamin Grena, a recent graduate in
materials science and engineering, referred to it as making "mille
feuille," (literally, "a thousand leaves," the French name for a
Napoleon pastry). That method increased the conductivity of the polymer
by a factor of four or five, Park says. "That allowed us to reduce the
size of the electrodes by the same amount."
One immediate question that could be addressed through such fibers is
that of exactly how long it takes for the neurons to become
light-sensitized after injection of the genetic material. Such
determinations could only be made by crude approximations before, but
now could be pinpointed more clearly, the team says. The specific
sensitizing agent used in their initial tests turned out to produce
effects after about 11 days.
The team aims to reduce the width of the fibers further, to make
their properties even closer to those of the neural tissue. "The next
engineering challenge is to use material that is even softer, to really
match" the adjacent tissue, Park says. Already, though, dozens of
research teams around the world have been requesting samples of the new
fibers to test in their own research.
And for those 10% that have access to stroke care it is still a complete fucking failure. 'Happy talk' abounds because even these stroke experts are waiting for SOMEONE ELSE TO SOLVE THE PROBLEM.
Get cracking on these solutions because you are completely on your own to solve everything in stroke. With NO strategy and NO leadership nothing will get done for decades. 1. Only 10% of patients get to full recovery. 2.tPA only fully works to reverse the stroke 12% of the time. 3. No protocols to prevent your 33% dementia chance post-stroke from an Australian study. 4. Nothing to alleviate your fatigue. 5. Nothing that will cure your spasticity. 6. Nothing on cognitive training unless you find this yourself. 7. No published stroke protocols. 8. No way to compare your stroke hospital results vs. other stroke hospitals.
Stroke
experts gathered at the International Stroke Conference in Houston Feb.
23 to discuss how many parts of the world have limited access to
technologies and treatments for stroke.
About 90 percent of the world’s population has no access or very
limited access to stroke resources that have emerged in the last 20
years, according to Werner Hacke, MD, PhD, a senior professor of
neurology at the University of Heidelberg in Germany and the president
of the World Stroke Organization.
“Advances in stroke treatment and prevention are often expensive and
available only to people living in special areas in high-income
regions,” he said in a statement from the American Heart Association.
Many areas where stroke treatment and prevention are limited are
communities with limited healthcare access in general. Some don’t even
have access to CT scanners. Additionally, many people living in those
areas are not educated on what stroke symptoms look like and what they
should do in the event of stroke.
The physicians who met at the conference shared their ideas and
strategies for developing stroke care protocols across economic
spectrums. One area where incidence of strokes is increasing is Eastern
Europe.
“Stroke is a rapidly advancing field, but it leaves many people
behind,” Hacke said. “This session addresses these challenges in stroke
care, as well as progress around the world. It will be valuable to
practitioners, policymakers, nurses and anybody interested in improving
the treatment of acute stroke.”
Just when the fuck will this become a standard protocol? It has even been tested in humans. Does no one ever take a stand and put protocols out there for real world use? It always seems to be more study needed.
Note that this study was
published as an abstract and presented at a conference. These data and
conclusions should be considered to be preliminary until published in a
peer-reviewed journal.
Vagal nerve stimulation (VNS) plus
rehabilitation significantly improved arm function in stroke patients
compared to rehabilitation alone 90 days after completion of treatment,
in a small, randomized, sham-controlled pilot trial.
Note that
arm weakness after stroke affects 75% of patients, persists in 50%, and
predicts poor quality of life, according to prior published research.
HOUSTON -- Although a small trial
of vagus nerve stimulation (VNS) to revive lost arm function in stroke
patients missed its early primary endpoint, significant functional
differences were seen at longer intervals, researchers reported here.
In the randomized, sham-controlled pilot trial, there were no
significant differences between groups in change in Upper Extremity Fugl
Meyer Assessment (FMA) scores after 6 weeks of stimulation plus
rehabilitation (mean change 7.6 points for VNS and 5.3 points for
controls, P=0.26), according to Jesse Dawson, MD, of the University of Glasgow.
But those scores diverged significantly 90 days after the stimulation and rehabilitation therapy was over (9.5 versus 3.8, P=0.05), Dawson reported during a press briefing at the International Stroke Conference.
"All in all, we feel this is promising," Dawson said. "I think we've
shown that the technique is acceptably safe. Crucially, I think we have
shown that we can deliver a partially home-based brain stimulation
technique."
Dawson's group enrolled 17 ischemic stroke patients, mean age 60 and
with an even gender divide, who had moderate-to-severe arm weakness as
assessed by FMA scores of 20 to 50.
All of them received the device -- the intervention arm received
stimulation plus rehabilitation, performed for 6 weeks in the clinic and
with 30-minutes daily of home exercises. Controls received sham
stimulation plus rehab, and were able to cross-over and receive
stimulation after the study was complete.
The stimulation was delivered at 0.5 seconds of 0.8 milliamps (mA)
per movement, with about 400 stimulations per session, and controls were
given 0 mA. Dawson noted that to optimize blinding, they initially gave
all participants some stimulation, as some evidence has suggested that
some people feel the stimulation at first but it wears off.
"When
we asked people which group they thought they were in, 33% were right.
It should have been 50%, so we feel like our paradigm worked," he said.
Participants, therapists, and assessors were blinded through 90 days after the therapy was completed.
Overall, there were three serious adverse events: one infection, one
shortness of breath and dysphagia due to intubation, and one vocal cord
paralysis. The former two cases resolved, but the patient who had vocal
cord paralysis is still recovering, the researchers said. Philip Gorelick, MD, MPH,
of Michigan State University in Grand Rapids said that while the
"target benefit is the release of neuroplastic substances, there are
going to be other effects because you're stimulating the vagal nerve."
Gorelick, , who was not involved in this study but is conducting
related work with VNS, said the stimulation should be monitored to
ensure that it's reaching the target area, particularly when patients
are performing therapeutic exercises at home.
Other
adverse events in the trial included typical surgical events such as
bruising, pain, swelling, and scarring. There were no cardiac events,
Dawson said.
In addition to missing the primary endpoint in the shorter term, but
garnering improvements at 90 days, there was a significantly higher
responder rate in the intervention group at that time point (88% versus
33%, P=0.05).
The responder rate was also higher immediately after therapy, but not significantly so (75% versus 33%).
There were also non-significant trends in the right direction for
change in the Wolf Motor Function Test (WMFT) both in the short term
(0.25 versus 0.13, P=0.26) and at 90 days (0.36 versus 0.04, P=0.07), they reported.
When sham stimulation patients were allowed to cross over, FMA scores improved significantly, by a mean of about 8 points (P=0.002), and there was a similar significant pattern for WMFT scores, Dawson said.
Between this study and earlier research,
Dawson said there appears to be about a 9-point change in FMA scores,
"which I think most people would regard as clinically important."
The 9-point change is relative to where patients started at baseline,
he explained. For those who have extremely poor function, they might be
able to regain some grasp function so they could pick up a plate. If
they were able to grasp when they started the trial, they might be able
to regain some fine motor function, he said.
Gorelick agreed that the change would likely be clinically significant, but he also called for quality-of-life data.
"When we a see jump like that, we think it's safe to conclude there
is clinical significance, but additional information about
quality-of-life and some other scales could be very helpful in cementing
the benefit," he said.
He also said that functional MRI data, to illustrate the
neuroplasticity remodeling that is supposed to taking place in the brain
because of the stimulation, would be an important part of the picture. A
120-patient study will begin in summer 2017. Asked if his group is
considering changing the timing of the primary endpoint for the next
trial, Dawson said they believe that, with a larger number of patients,
they should be able to detect a benefit early on.
"We would like to show that there's an effect with just 6 weeks of
therapy," he said, "but it does seem like an investment in longer
treatment would be worth taking."
The study was supported by MicroTransponder. Some co-authors are company employees.
Dawson and co-authors disclosed relevant relationships with MicroTransponder.
Researchers analyzed nutrition studies in a new review
published today in the Journal of the American College of Cardiology,
which intends to cut through the confusion about the best dietary
patterns to reduce heart disease. The review concludes current evidence
strongly supports eating plenty of fruits, vegetables, whole grains,
legumes, and nuts in moderation. Although more controversial, some
heart-healthy diets may also include very limited quantities of lean
meat, fish, low-fat and nonfat dairy products, and liquid vegetable
oils.
“There is a great amount of misinformation about nutrition fads,
including antioxidant pills, juicing and gluten-free diets,” said Andrew
Freeman, MD, director of cardiovascular prevention and wellness in the
division of cardiology at National Jewish Health in Denver and the
paper’s lead author. “However, there are a number of dietary patterns
that have clearly been demonstrated to reduce the risk of many chronic
diseases, including coronary heart disease.”
The review examined several of these dietary patterns as well as
“hypes and controversies” surrounding nutrition to provide clinicians
with information to aid in discussions with patients about dietary
habits.
“There is a growing consensus that a predominantly plant-based diet
that emphasizes green, leafy vegetables, whole grains, legumes and fruit
is where the best improvements are seen in heart health,” Freeman said.
Other nutrition topics covered in the review include:
Eggs and cholesterol. Although a government report issued in 2015
dropped specific recommendations about upper limits for cholesterol
consumption, the review concludes, “it remains prudent to advise
patients to significantly limit intake of dietary cholesterol in the
form of eggs or any high cholesterol foods to as little as possible.”
Vegetable oils. Coconut oil and palm oil should be discouraged due to
limited data supporting routine use. The most heart-healthy oil is
olive oil, though perhaps in moderation as it is still higher calorie,
research suggests.
Berries and antioxidant supplementation. Fruits and vegetables are
the healthiest and most beneficial source of antioxidants to reduce
heart disease risk. There is no compelling evidence adding high-dose
antioxidant dietary supplements benefits heart health.
Nuts. Nuts can be part of a heart-healthy diet. But beware of consuming too many, because nuts are high in calories.
Juicing. While the fruits and vegetables contained in juices are
heart-healthy, the process of juicing concentrates calories, which makes
it is much easier to ingest too many. Eating whole fruits and
vegetables is preferred, with juicing primarily reserved for situations
when daily intake of vegetables and fruits is inadequate. If you do
juice, avoid adding extra sugar by putting in honey, to minimize
calories.
Gluten. People who have celiac disease or other gluten sensitivity
must avoid gluten—wheat, barley and rye. For patients who don’t have any
gluten sensitivities, many of the claims for health benefits of a
gluten-free diet are unsubstantiated, the researchers conclude.
The authors also addressed why there can be confusion surrounding
nutrition studies. According to Freeman, many of these studies are
funded and/or influenced by the food industry and may have some bias.
“In addition, it’s very hard to separate the effects of specific
nutrients in a food. For example, an apple contains many components
including proteins, vitamins and fiber,” he said.
Many people who eat a healthy diet also have other healthy lifestyle
behaviors, such as regular physical activity, getting enough sleep, and
not smoking, and it can be hard to pinpoint the diet’s effect separate
from these other behaviors.
“And some nutrition studies tend to be based on surveys that rely on
people’s memories of what they ate, which isn’t always reliable,”
Freeman said.
“The founder of modern medicine, Hippocrates, said, ‘Let food be thy
medicine,’” Freeman said. “But the vast majority of doctors have little
nutrition training. If we can get doctors, and especially cardiologists,
to understand the value of nutrition in medical practice, we can have a
greater impact on reducing heart disease, and it is certainly
cost-effective.”
The authors have several disclosures to report, which are listed on the document.
Full bibliographic informationTrending Cardiovascular Nutrition Controversies
Andrew
M. Freeman, MD, Pamela B. Morris, MD, Neal Barnard, MD, Caldwell B.
Esselstyn, MD, Emilio Ros, MD, PHD,e Arthur Agatston, MD, Stephen
Devries, MD, James O’Keefe, MD, Michael Miller, MD, Dean Ornish, MD, Kim
Williams, MD, Penny Kris-Etherton, PHD
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Transcranial
direct current stimulation (tDCS), a form of noninvasive brain
stimulation originally studied for its effect on motor limb physiology,1 has been investigated for its use in the treatment of aphasia since 2008.2–3
The experimental use of tDCS for aphasia, however, began differently
from those paradigms established for poststroke motor recovery, both
conceptually and in method. Not only is aphasia research a relative
newcomer to the field of tDCS experimentation, it has thus far been
somewhat of an outlier in its limited use of tDCS autonomously.
Theoretically
understood to be vastly more complex than our intricate motor systems,
cortical language representation has most recently been conceptualized
as a dual stream, diffuse network,4–6 with language processing subcomponents evolved from nonlinguistic primates.7,8
In the dual stream model, human language functions are lateralized
primarily in the left hemisphere, with Broca’s area comprising the left
complement of a bilateral dorsal stream network devoted to naming and
articulation. Conversely, Wernicke’s area constitutes the origin of a
bilateral ventral stream in which semantic meaning is attached to
components of speech sounds.6,9–21
Additional activation in homologous right hemisphere language areas
seems to be determined by lexical necessity, with increased articulatory
demands activated within the bilateral dorsal stream and the decoding
of unfamiliar words activated in the bilateral ventral stream network.9
Complex as it may be to optimally prime the motor cortex for poststroke
limb rehabilitation using tDCS, it may be considered even more
challenging to modulate the cortical plexus which encodes and produces
language in all of its richness. The theoretical mechanisms of brain
activation during tDCS protocols suggest that tDCS primes the brain for
enhanced outcomes in behavioral therapies,22 which may have led to the appeal of combining methods concurrently. The …
Steven C. Cramer, Steven L. Wolf, Harold P. Adams, Daofen Chen, Alexander W. Dromerick, Kari Dunning, Caitlyn Ellerbe, Andrew Grande, Scott Janis, Maarten G. Lansberg, Ronald M. Lazar, Yuko Y. Palesch, Lorie Richards, Elliot Roth, Sean I. Savitz, Lawrence R. Wechsler, Max Wintermark, Joseph P. Broderick
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Stroke
is the second leading cause of death and the third leading cause of
disability-adjusted life years worldwide. Although numerous therapies
have been developed over the past 10 years to treat acute ischemic
stroke, the stark reality remains that only 5% of these patients are so
treated in the United States,1
in part, because of treatment window times <3 to 6 hours post-onset,
and many of these 5% nonetheless have significant long-term disability.
Acute treatment options after hemorrhagic stroke remain limited.2
In
parallel with efforts to further develop acute stroke interventions,
researchers are studying recovery and rehabilitation treatments, which
can have a treatment time window measured in days, weeks, or months
poststroke. To achieve this goal, therapies aim to maximize function in
brain areas that survive the stroke or provide compensatory approaches
to improve overall function. Strategies targeting recovery and
rehabilitation must be seen as distinct from acute stroke therapies,
such as reperfusion or neuroprotection, where the strategy is to limit
the severity of ischemic injury, including preserving penumbral tissue
and reducing infarct size.
Preclinical and translational
research have successfully identified numerous molecular and
physiological events spontaneously arising in the nervous system during
the days-to-weeks after an infarct, and, subsequently, potential
restorative therapies that target these events to improve long-term
behavioral outcomes.3,4
In parallel, a burgeoning volume of data from human subjects has
emerged regarding mechanisms of recovery from stroke. Together, these
efforts inform translation into clinical studies for several classes of
therapy, including small molecules, growth factors, stem cells,
monoclonal antibodies, brain stimulation, robotics and other devices,
cognitive strategies, intensive training, and telerehabilitation.5,6
The
majority of patients with stroke survive the initial event but go on to
live with significant disability for many years. Indeed, there are >7 million stroke survivors …
Jessalyn K. Holodinsky, Noreen Kamal, Alexis T. Wilson, Michael D. Hill, Mayank Goyal
https://doi.org/10.1161/STROKEAHA.116.015951
Stroke. 2017;48:808-812
Originally published February 13, 2017
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The
manner in which information is presented can profoundly affect the
interpretation of that information and, consequently, any action taken.
As an illustrative example, let us assume that swimming pools across the
country have to report the time it takes to rescue a child who is
drowning. As a parent, would you be satisfied if the median time to
rescue a drowning child was 30 seconds? Knowing that a lifeguard could
reach your child in only half a minute may be comforting. However, this
comfort likely would not last if you were then informed that the 90th
percentile is 6 minutes, a time which is likely life-threatening. We
argue here that acute ischemic stroke treatment faces a similar
reporting issue and that we should be doing more to acknowledge and
improve the 90th percentile for stroke patients.
We
recommend that investigators report interval times with the 90th
percentile, in addition to median and interquartile range, in their
primary results on paper and at presentation. In the long run, this
change would allow us to focus on ensuring that the majority of patients
are treated within an acceptable time frame, rather than only 50% of
patients. Additionally, efforts tailored to improving the 90th
percentile would result in improved systems of care and stroke outcomes.
Based on data from recent endovascular trials, it is absolutely clear that when it comes to stroke treatment, time is brain.1–5 The longer the time from onset to reperfusion, the lower the likelihood of good outcome.6 The effect of time delay is even more pronounced when one considers onset to randomization times in endovascular trials.1–5
This is not because of physiological factors; rather, it is the result
of these trials overtly selecting patients based on favorable imaging.(cherry picking)
In all of …
I would argue that your conclusion is wrong, these people just had better spontaneous recovery. The people who can stand intensive early rehab were likely less disabled by the stroke to begin with. I don't see any objective diagnosis of stroke damage here so this research is not repeatable. http://stroke.ahajournals.org/content/48/3/740?etoc=
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Abstract
Background and Purpose—We
aimed to examine the concurrent effects of timing and intensity of
rehabilitation on improving activities of daily living (ADL) among
patients with ischemic stroke.
Methods—Using
the Japanese Diagnosis Procedure Combination inpatient database, we
retrospectively analyzed consecutive patients with ischemic stroke at
admission who received rehabilitation (n=100 719) from April 2012 to
March 2014. Early rehabilitation was defined as that starting within 3
days after admission. The average rehabilitation intensity per day was
calculated as the total units of rehabilitation during hospitalization
divided by the length of hospital stay. A multivariable logistic
regression analysis with multiple imputation and an instrumental
variable analysis were performed to examine the association of early and
intensive rehabilitation with the proportion of improved ADL score.
Results—The
proportion of improved ADL score was higher in the early and intensive
rehabilitation group. The multivariable logistic regression analysis
showed that significant improvements in ADL were observed for early
rehabilitation (odds ratio: 1.08; 95% confidence interval: 1.04–1.13; P<0.01) and intensive rehabilitation of >5.0 U/d (odds ratio: 1.87; 95% confidence interval: 1.69–2.07; P<0.01).
The instrumental variable analysis showed that an increased proportion
of improved ADL was associated with early rehabilitation (risk
difference: 2.8%; 95% confidence interval: 2.0–3.4%; P<0.001) and intensive rehabilitation (risk difference: 5.6%; 95% confidence interval: 4.6–6.6%; P<0.001).
Conclusions—The
present results suggested that early and intensive rehabilitation
improved ADL during hospitalization in patients with ischemic stroke.
Andrew Bivard, Christopher Levi, Longting Lin, Xin Cheng, Richard Aviv, Neil J. Spratt, Min Lou, Tim Kleinig, Billy O’Brien, Kenneth Butcher, Jingfen Zhang, Jim Jannes, Qiang Dong, Mark Parsons
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Abstract
Background and Purpose—Advanced
imaging to identify tissue pathophysiology may provide more accurate
prognostication than the clinical measures used currently in stroke.
This study aimed to derive and validate a predictive model for
functional outcome based on acute clinical and advanced imaging
measures.
Methods—A
database of prospectively collected sub-4.5 hour patients with ischemic
stroke being assessed for thrombolysis from 5 centers who had computed
tomographic perfusion and computed tomographic angiography before a
treatment decision was assessed. Individual variable cut points were
derived from a classification and regression tree analysis. The optimal
cut points for each assessment variable were then used in a backward
logic regression to predict modified Rankin scale (mRS) score of 0 to 1
and 5 to 6. The variables remaining in the models were then assessed
using a receiver operating characteristic curve analysis.
Results—Overall,
1519 patients were included in the study, 635 in the derivation cohort
and 884 in the validation cohort. The model was highly accurate at
predicting mRS score of 0 to 1 in all patients considered for
thrombolysis therapy (area under the curve [AUC] 0.91), those who were
treated (AUC 0.88) and those with recanalization (AUC 0.89). Next, the
model was highly accurate at predicting mRS score of 5 to 6 in all
patients considered for thrombolysis therapy (AUC 0.91), those who were
treated (0.89) and those with recanalization (AUC 0.91). The odds ratio
of thrombolysed patients who met the model criteria achieving mRS score
of 0 to 1 was 17.89 (4.59–36.35, P<0.001) and for mRS score of 5 to 6 was 8.23 (2.57–26.97, P<0.001).
Conclusions—This study has derived and validated a highly accurate model at predicting patient outcome after ischemic stroke.
