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.
How is your doctor making sure you have the ability to stay socially engaged even after your stroke? ANYTHING AT ALL? 100% recovery would be the best solution but I know your doctor will fail at that. I joined numerous Meetup groups. Of the various stroke support groups I attended most were of the 'Woe is me' and useless. The one good one had us bowling every week and I became quite proficient with a number of 200+ games. You do expect your doctor to have protocols to prevent your cognitive decline and chance of dementia, don't you? Or are you giving a pass to your possibly incompetent doctor?
Summary: An
association has been discovered between cognitive decline and social
engagement in older adults. Older people who are less socially active
have a greater accumulation of amyloid beta and increased cognitive
decline over a three-year span, compared to more socially active peers.
Source: Brigham and Women’s Hospital Social relationships are essential to aging well; research
has shown an association between lack of social engagement and increased
risk of dementia. A new study by investigators from Brigham and Women’s
Hospital found that higher brain amyloid-β in combination with lower
social engagement in elderly men and women was associated with greater
cognitive decline over three years. The results of the study were
published last month in the American Journal of Geriatric Psychiatry.
“Social engagement and cognitive function are related to one another
and appear to decline together,” said senior author Nancy Donovan, MD,
chief of the Division of Geriatric Psychiatry at the Brigham. “This
means that social engagement may be an important marker of resilience or
vulnerability in older adults at risk of cognitive impairment.”
The investigators sampled 217 men and women enrolled in the Harvard
Aging Brain Study, a longitudinal observational study looking for early
neurobiological and clinical signs of Alzheimer’s disease. The
participants, aged 63-89, were cognitively normal, but some individuals
showed high levels of amyloid-β protein, a pathologic hallmark of
Alzheimer’s disease detected with neuroimaging techniques.
The investigators used standard questionnaires and examinations to
assess participants’ social engagement (including activities such as
spending time with friends and family and doing volunteer work) and
cognitive performance at baseline and three years later.
Well duh, the lack of effectiveness is because
the research out there never had an objective starting point so you
didn't know which patient the rehab worked on and could map the stroke
protocols to objective damage. This is so fucking easy to understand,
get the hell out of the way and let stroke survivors run stroke.
The existing approach for brain stimulation to rehabilitate
patients after a stroke does not take into account the diversity of
lesions and the individual characteristics of patients' brains, a study
has found.
In recent decades, non-invasive neuromodulation methods
such as electric and magnetic stimulation of various parts of the
nervous system have been increasingly used to rehabilitate patients
after a stroke.
Stimulation selectively affects different parts of the brain, which
allows you to functionally enhance activity in some areas while
suppressing unwanted processes in others that impede the restoration of
brain functions.
This is a promising mean of rehabilitation after a stroke. However, its results in patients remain highly variable.
Authors
of the study, which was published in the journal 'Frontiers in
Neurology', argued that the main reason for the lack of effectiveness in
neuromodulation approaches after a stroke is an inadequate selection of
patients for the application of a particular brain stimulation
technique.
They said the existing approach does not take into
account the diversity of lesions after a stroke and the variability of
individual responses to brain stimulation as a whole.
The researchers have proposed two criteria for selecting the optimal brain stimulation strategy.
The
first is an analysis of the interactions between the hemispheres. Now,
all patients, regardless of the severity of injury after a stroke, are
offered a relatively standard treatment regimen. This approach relies on
the idea of interhemispheric competition.
"For a long time, it
was believed that when one hemisphere is bad, the second, instead of
helping it, suppresses it even more," said
Maria Nazarova, researcher at the HSE Institute of Cognitive Neurosciences.
"In
this regard, the suppression of the activity of the "unaffected"
hemisphere should help restore the affected side of the brain. However,
the fact is that this particular scheme does not work in many patients
after a stroke. Each time it is necessary to check what the impact of
the unaffected hemisphere is -- whether it is suppressive or
activating," she said.
According to the researchers, the second criterion is the neuronal phenotype.
This is an individual characteristic of the activity of the brain, which is 'unique to each person like their fingerprints'.
Such
a phenotype is determined, firstly, by the ability of the brain to
build effective structural and functional connections between different
areas (connectivity).
Secondly, the individual characteristics of
neuronal dynamics, including its ability to reach a critical state. This
is the state of the neuronal system in which it is the most plastic and
capable of change.
(This story has not been edited by Business Standard staff and is auto-generated from a syndicated feed.)
So human clinical testing needed. What is your doctor and hospital doing to facilitate that? ANYTHING AT ALL? Are
your doctor and hospital responsible for anything in stroke? Maybe
burying their heads in the sand so they don't have to tackle any of the BHAGs(Big Hairy Audacious Goals) of 100% recovery for all survivors.
Was any followup done from Sept. 2017 when this came out? NO? then get your stroke hospital president and board of directors fired for incompetence.
An experimental treatment for stroke can help restore
movement and reduce brain cell damage in mice, a study has found, paving
the way for new therapies to help victims of debilitating brain
injuries recover.
Stroke -- a condition in which poor blood flow
to the brain results in cell death -- requires time-sensitive treatment,
researchers said.
Clotting factors like thrombin are commonly administered to patients,
but there are many other stroke-related signs that can be targeted,
such as swelling and ion imbalances in the surrounding fluids.
The
study, published in the journal Proceedings of the National Academy of
Sciences, shows that brain fluids can be normalised with adrenergic
receptor antagonists -- a combination of drugs to block the activity of
adrenaline in the brain.
The experimental treatment for stroke aided motor recovery and reduced cell death in mice, scientists said.
A
major consequence of stroke is an immediate imbalance in the ion
concentrations of fluids that bathe brain cells. Potassium levels spike
and fluid accumulates, which leads to swelling, a major cause of stroke
injury.
"We know that the water dynamics in the brain immediately
during and after a stroke are critical, so we focused on the pathways
that move fluids in and out of cells," said Hiromu Monai of the RIKEN
Center for Brain Science and Ochanomizu University in Japan.
One
way to lower potassium and get neurons active again is by administering
adrenergic receptor (AdR) antagonists, drugs that counteract the
electrical and chemical disturbance that accompanies a stroke.
These
antagonist drugs have been found to promote fluid exchange in normal
brains, according to Maiken Nedergaard of the University of Rochester
Medical Center in the US.
A cocktail of AdR blockers was successful in reducing both the area of tissue damage and potassium levels in stroked mice.
Moreover,
even one or two hours post-stroke, administration of AdR blockers was
effective in stopping the infarct from spreading. Mice were also able to
recover the use of their forepaw much more quickly when treated with
AdR blockers.
The researchers found that levels of a water channel called aquaporin 4 were lower following a stroke.
"We think that preserving aquaporin levels is critical to protecting brain tissue during stroke," said Monai.
To test this idea, they used genetically engineered mice that lacked the aquaporin 4 water channel.
These
mice did not benefit from AdR blocker treatment and their brain
potassium levels remained high after stroke, supporting the idea that
the neuroprotective effect occurs through the action of aquaporin 4
water channels.
"Keeping potassium levels in balance is an
alternative therapeutic strategy for stroke, and we found that
adrenergic receptor blockers promote this normalization," said Monai.
"Recovering
motor function following a stroke is so important, and we also saw
improvements in the mice treated with AdR blockers," he said.
(This story has not been edited by Business Standard staff and is auto-generated from a syndicated feed.)
So human clinical testing needed. What is your doctor and hospital doing to facilitate that? ANYTHING AT ALL? Are
your doctor and hospital responsible for anything in stroke? Maybe
burying their heads in the sand so they don't have to tackle any of the BHAGs(Big Hairy Audacious Goals) of 100% recovery for all survivors.
IANS |
New York Last Updated at April 15, 2019 17:35 IST
Researchers have found that a gene could help the brain heal itself after a stroke or any other head-related injuries.
The study, published in Cell Reports, suggested that a dose of the TRIM9
gene could reduce brain swelling after stroke, prevent damage following
a blow to the head (concussion) or encephalitis, which is the
inflammation of the brain.In addition, in a lab model, the researchers from the University of
Southern California found that older brains with low TRIM9 levels -- or
engineered brains missing the TRIM9 gene entirely -- were prone to
extensive swelling following a stroke.
The is because TRIM9 is abundant in the youthful brain but grows scarce with age.
On the other hand, when the team used a harmless virus to carry a dose
of the gene directly into TRIM9-deficient brains, the swelling decreased
dramatically and recovery improved, the findings further revealed.
It is unlikely that gene therapy delivered by viruses will become the
go-to treatment for strokes, head injuries or encephalitis as the best
shot at treating stroke is within the first 30 minutes to one hour, said
lead author Jae Jung at the varsity.
Jung further added that not all inflammation in the brain is bad as it
plays a role in fighting infection and helps clear away dead tissue.
However, inflammation for a long duration could lead to the death of
neurons.
--IANS
pb/vd
(This story has not been edited by Business Standard staff and is auto-generated from a syndicated feed.)
All
human experience is rooted in the brain, but we just barely understand
how it works. That’s partially because it’s hard to study: Scientists
can’t just run experiments on living brains, and experiments on animal
brains don’t always translate to humans. That’s why researchers
developed the brain organoid, an artificially grown, three-dimensional cluster of human neurons that faithfully mimics brain development — and, as Japanese scientists reported Wednesday in Cell Stem Cell, the neural activity of a living brain as well.
Neurons
in a living brain respond to stimuli by “firing” off electrical
impulses, which they use to communicate with one another and with other
parts of the body. The scientists behind the new paper discovered that
the brain organoids they grew from scratch in their lab also started to
exhibit synchronized activity, just like neurons in an actual brain.
That team included first and co-corresponding author Hideya Sakaguchi, Ph.D., a postdoctoral fellow at Kyoto University currently at the Salk Institute.
“I
was very excited to see some of the neurons activated at the same time
robustly at first,” Sakaguchi, who did the first of his experiments in
December 2016, tells Inverse. “Neurons first show individual
activities, but as they form networks and connections between other
neurons, they start to show synchronized activities.”
This,
he explains, is the basis of human brain function. But he’s not worried
that his organoids are at any risk of becoming conscious.
Why Brain Activity Matters
In
1949, the Canadian neuropsychologist Donald Hebb, Ph.D., introduced the
Cell Assembly Hypothesis, which posited that synchronized neural
activity was the basis for various brain functions, including memory. In
1992, the authors of a Sciencereport
put it more succinctly: “Neurons wire together if they fire together.”
Using their new technique for measuring brain cell activity, Sakaguchi
and his team found that brain organoids do the same, even if they’re
grown from scratch in a dish.
Their “mini brains”
were technically “cerebral organoids,” made from the cells that compose
the region of the brain known as the cerebrum. They started out as
clusters of stem cells raised in a special medium designed to support
brain development, eventually growing into organoids with a similar
structure as a real-life cerebrum.
Then,
Sakaguchi and his team pulled out some neurons from the organoids and
grew them separately, in hopes that this new culture, called a functional neural network,
would last longer than the full mini brain and would be less
challenging for visualizing dynamic function. It was in this simpler
culture that the team watched the neurons cluster and self-organize,
spontaneously creating the structure that would support the synchronized
activity. Then, “at last,” says Sakaguchi, “I saw very interesting
neural function via imaging.”
“The activity in a
dish is still preliminary compared with real brain,” he says, “and I
think the activity that we detect might correspond to very early stage
of cerebral development in a brain.”
It isn’t, he assures Inverse, evidence that the brain is thinking.
Why Brain Organoids Can’t Be Conscious
Growing human brain cells is controversial in part because some people worry that consciousness may arise from them, as “brain-in-a-vat”
thought experiments have proposed. If the brain cells we grow develop
consciousness, will we be any better than the evil AI overlords in the Matrix, placating living brains trapped in laboratories with virtual reality?
Sakaguchi
explains that even though the brain organoids are showing signs of
spontaneous activity, they are unlikely to develop consciousness because
they lack the ability to be stimulated, unlike living brains attached
to a body that senses the world.
“It is very
difficult to know they are thinking or feeling,” says Sakaguchi. “But we
think cerebral organoids without input and output system will not have
consciousness since consciousness require subjective experience.”
The real reason is because there is nothing even remotely close to getting you 100% recovered. And no one is working on that, so prevention is the only message possible. What needs to be solved here:
Nihilism in stroke for the complete list of what still needs to be fixed.
True stroke leaders would be working on those, but NO, lazy press releases are their only response. Nothing in the current prevention list would have even remotely suggested I would have a stroke at age 50 thirteen years ago.
The big statistic most of us hear about stroke is that our risk
doubles every decade after age 55. But earlier this year, actor Luke
Perry and director John Singleton died of stroke. Perry was 52,
Singleton just 51.
Last year, Olympic sprinter Michael Johnson — once known as “the
fastest man in the world”— survived a stroke at age 50. So, it appears waiting until age 55 to think about stroke could be deadly.
Are More Midlife Adults Having Strokes?
A 2017 study by researchers at the University of Michigan and the
Veterans Affairs Healthcare System’s Department of Neurology in Ann
Arbor, Mich., found that among people age 45 to 54, the rate of
hospitalization for the most common type of stroke rose more than 20% from 2003 to 2012.
But the study’s finding doesn’t necessarily mean that more people are
having strokes younger, says Dr. Koto Ishida, medical director at the
New York University Langone’s Comprehensive Stroke Center. “Rates aren’t
necessarily increasing, but awareness is,” she says.
About 80% of first-time stroke victims of any age have high blood pressure.
In 2003, the American Stroke Association launched a warning signs
awareness campaign. With increased awareness, more potential stroke
victims know to seek help sooner.
Also, Ishida says, diagnostic methods changed during the Michigan
study’s time period, so some 2012 stroke victims might have been
classified as something else in 2003.
One thing that does seem to be happening in people at younger ages:
more risk factors for stroke, including obesity, high blood pressure,
elevated cholesterol, coronary artery disease and diabetes. The Michigan
study found that the number of stroke victims age 45 to 54 with three
to five risk factors rose by more than 70%.
“We’re definitely seeing these risk factors younger,” says Ishida.
“We call many of them ‘silent killers.’ A lot of people come to us in
their forties and fifties believing they were healthy until now. But you
could’ve had high blood pressure for ten years and not known it.” About
80% of first-time stroke victims of any age have high blood pressure.
Stroke Risk and Prevention
Because risk factors like high blood pressure or cholesterol don’t
show symptoms until something like a stroke hits, an annual physical
exam is the most important thing people can do to prevent one, Ishida
says. That gives your doctor the chance to monitor you and help you lower elevated blood pressure or cholesterol to a less risky level.
There are some risk factors that you can’t change, however, like your
family history. “Younger strokes and younger risk factors run in
families,” Ishida says, adding that you should tell your doctor if
younger people in your family have died of stroke, so they will know to
start screening you sooner.
Race also matters when it comes to stroke: The risk of stroke among
blacks is nearly twice as high as for whites, and blacks tend to have
strokes younger.
Gender is another factor: The Michigan study found that among people
age 45 to 54, nearly 30% more men than women were hospitalized for
stroke.
But the good news is, up to 80% of strokes in the U.S. are preventable, according to the Centers for Disease Control and Prevention (CDC). These lifestyle changes can lower your risk of stroke:
Quit smoking. Smokers are two to four times more likely than non-smokers to have a stroke.
Lose weight. Obesity increases your risk for high blood pressure, diabetes and other key risk factors for stroke.
Drink less alcohol. It can raise your blood pressure. The CDC recommends men have no more than two drinks a day, and women just one.
‘BE FAST’ Could Save a Life
Stroke is the fifth-leading cause of death in the U.S., but far more people survive stroke than die of it. As many as nine out of 10 survivors have some paralysis immediately after.
Thanks to medical advances in emergency treatment, recognizing a
stroke immediately could make the difference between a full recovery and
decades of living with a stroke-related disability. But for people
under 55, stroke isn’t often top of mind.
“Every minute when you have complete blockage of blood flow to the
brain, two million brain cells are irreversibly killed,” Ishida says.
“If you wait and come in the next morning, it takes treatments off the
table.”
The sudden onset of symptoms is a hallmark of stroke — there aren’t a
lot of other things that happen so quickly, says Ishida. A sudden
severe headache can be a symptom, but otherwise there usually isn’t much
pain. “That’s a downside for us in the stroke world,” Ishida says.
“Pain is a good motivator to get people to the ER.”
The American Stroke Association and National Stroke Association both suggest the acronym “FAST” to help you remember the key symptoms of stroke:
Face: Try to smile. Is one side droopy?
Arms: Lift both arms. Is one side weaker than the other?
Speech: Are you having trouble getting words out, slurring or having difficulty understanding others?
Time: Get treatment as quickly as possible. If the answer is Yes to any of the above questions, call 911 immediately.
While FAST is handy, it’s far from complete. Ishida likes to add the word BE before FAST to cover more possible signs:
Balance: Are you feeling dizzy or struggling to keep your body steady?
Eyes: Do you have a sudden problem with one or both eyes or double vision?
Whatever you do, don’t attempt to treat symptoms yourself. The two primary types of stroke have identical symptoms but do virtually opposite things to your brain.
The most common type, ischemic, happens when a blood clot cuts off blood flow to your brain.
Hemorrhagic strokes happen when a weakened blood vessel ruptures and
blood floods into surrounding brain tissue. Since you don’t know what
type of stroke you’re facing, guessing at treatment could be
catastrophic.
Bottom line, says Ishida: “If you’re having sudden onset of one of
those symptoms, stroke should be top of mind, no matter your age.”
It is your doctor's responsibility to get you recovered enough by the time you leave the hospital to do enough exercise to get these benefits. And your doctor's responsibility to create an exact exercise protocol for these benefits.
A growing body of research shows there are many ways to lower
Alzheimer's risk. What are they? Which one is best? See what Cleveland
Clinic's Aging Survey revealed.
LEXINGTON, Ky. (May 17, 2016) --
A group of researchers led by Nathan Johnson PT, DPT, PhD of the
University of Kentucky College of Health Sciences, was able to
demonstrate a positive correlation between fitness and blood flow to
areas of the brain where the hallmark tangles and plaques of AD
pathology are usually first detected.
Continued below video...
Thirty men and women ages 59-69 were put through treadmill fitness
assessments and ultrasounds of the heart. Then they received brain scans
to look for blood flow to certain areas of the brain.
Continued below ad...
"We set out to characterize the relationship between heart function,
fitness, and cerebral blood flow, which no other study had explored to
date," Johnson said. "In other words, if you're in good physical shape,
does that improve blood flow to critical areas of the brain? And does
that improved blood flow provide some form of protection from dementia?"
The results showed blood flow to critical areas of the brain - and so
the supply of oxygen and vital nutrients - was higher in those who were
more physically fit.
In layman's terms, this study demonstrates that regular exercise at any age could keep the mind young, according to Johnson.
"Can we prove irrefutably that increased fitness will prevent
Alzheimer's disease? Not at this point," Johnson said. "But this is an
important first step towards demonstrating that being physically active
improves blood flow to the brain and confers some protection from
dementia, and conversely that people who live sedentary lifestyles,
especially those who are genetically predisposed to Alzheimer's, might
be more susceptible."
Since people who exercise frequently often have reduced arterial
stiffness, Johnson and his group postulate that regular physical
activity(We need to know exactly how much - A protocol) - regardless of age - maintains the integrity of the "pipes"
that carry blood to the brain.
"In the mid-late 20th century, much of the research into dementias like
Alzheimer's focused on vascular contributions to disease, but the
discovery of amyloid plaques and tangles took prevailing research in a
different direction" Johnson said. "Research like this heralds a return
to the exploration of the ways the vascular system contributes to the
disease process."
Johnson's research, which was supported by a grant from the National
Institutes of Health CTSA (UL1TR000117) and the University of Kentucky's
Clinical Services Core, was published in NeuroImage.
Does your doctor have enough gumption and brains to try this on stroke patients maybe as a preventative to your likely chance of getting dementia? Before it is totally proven out?
I would suggest that we just hand all the problems in stroke over to MIT graduates and let them get a Nobel prize early in their career. A competent stroke leader would look at all these incredibly smart people needing a project to graduate with and hand them all the nihilism in stroke problems. But that will never occur. We have NO STROKE LEADERSHIP, stroke is totally rudderless.
Damn it all: stroke is easy; 5 steps. 1. Describe the problems exactly.
2. Write thousands of RFPs to researchers/MIT grads to solve those problems.
3. Fund them with foundation grants.
4. Write stroke rehab protocols based on the research.
5. Get the Nobel prize in medicine
MIT researchers substantially reduced beta-amyloid plaques in Alzheimer’s, using LED lights flickering at a specific frequency.
Helps Cells That Destroy Alzheimer's Plaque
This treatment appears to work by inducing brain waves known as gamma
oscillations, which the researchers discovered help the brain suppress
beta amyloid production and invigorate cells responsible for destroying
the plaques.
Further research will be needed to determine if a similar approach
could help Alzheimer’s patients, says Li-Huei Tsai, the Picower
Professor of Neuroscience, director of MIT’s Picower Institute for
Learning and Memory, and senior author of the study, which appears in
the online edition of Nature.
Article continued below video...
Researchers in Li-Huei Tsai's laboratory at the Picower
Institute for Learning and Memory have shown that disrupted gamma waves
in the brains of mice with Alzheimer’s disease can be corrected by
a unique non-invasive technique using flickering light.
Video: The Picower Institute for Learning and Memory
“It’s a big ‘if,’ because so many things have been shown to work in
mice, only to fail in humans,” Tsai says. “But if humans behave
similarly to mice in response to this treatment, I would say the
potential is just enormous, because it’s so noninvasive, and it’s so
accessible.”
Tsai and Ed Boyden, an associate professor of biological engineering
and brain and cognitive sciences at the MIT Media Lab and the McGovern
Institute for Brain Research, who is also an author of the Nature paper,
have started a company called Cognito Therapeutics to pursue tests in
humans. The paper’s lead authors are graduate student Hannah Iaccarino
and Media Lab research affiliate Annabelle Singer.
“This important announcement may herald a breakthrough in the
understanding and treatment of Alzheimer's disease, a terrible
affliction affecting millions of people and their families around the
world,” says Michael Sipser, dean of MIT’s School of Science. “Our MIT
scientists have opened the door to an entirely new direction of research
on this brain disorder and the mechanisms that may cause or prevent
it. I find it extremely exciting.”
Brain wave stimulation
Alzheimer’s disease, which affects more than 5 million people in the
United States, is characterized by beta amyloid plaques that are
suspected to be harmful to brain cells and to interfere with normal
brain function. Previous studies have hinted that Alzheimer’s patients
also have impaired gamma oscillations. These brain waves, which range
from 25 to 80 hertz (cycles per second), are believed to contribute to
normal brain functions such as attention, perception, and memory.
In a study of mice that were genetically programmed to develop
Alzheimer’s but did not yet show any plaque accumulation or behavioral
symptoms, Tsai and her colleagues found impaired gamma oscillations
during patterns of activity that are essential for learning and memory
while running a maze.
Next, the researchers stimulated gamma oscillations at 40 hertz in a
brain region called the hippocampus, which is critical in memory
formation and retrieval. These initial studies relied on a technique
known as optogenetics, co-pioneered by Boyden, which allows scientists
to control the activity of genetically modified neurons by shining light
on them. Using this approach, the researchers stimulated certain brain
cells known as interneurons, which then synchronize the gamma activity
of excitatory neurons.
40% to 50% Reduction
After an hour of stimulation at 40 hertz, the researchers found a 40 to
50 percent reduction in the levels of beta amyloid proteins in the
hippocampus. Stimulation at other frequencies, ranging from 20 to 80
hertz, did not produce this decline.
Tsai and colleagues then began to wonder if less-invasive techniques
might achieve the same effect. Tsai and Emery Brown, the Edward Hood
Taplin Professor of Medical Engineering and Computational Neuroscience, a
member of the Picower Institute, and an author of the paper, came up
with the idea of using an external stimulus — in this case, light — to
drive gamma oscillations in the brain. The researchers built a simple
device consisting of a strip of LEDs that can be programmed to flicker
at different frequencies.
Using this device, the researchers found that an hour of exposure to
light flickering at 40 hertz enhanced gamma oscillations and reduced
beta amyloid levels by half in the visual cortex of mice in the very
early stages of Alzheimer’s. However, the proteins returned to their
original levels within 24 hours.
The researchers then investigated whether a longer course of
treatment could reduce amyloid plaques in mice with more advanced
accumulation of amyloid plaques. After treating the mice for an hour a
day for seven days, both plaques and free-floating amyloid were markedly
reduced. The researchers are now trying to determine how long these
effects last.
Furthermore, the researchers found that gamma rhythms also reduced
another hallmark of Alzheimer’s disease: the abnormally modified Tau
protein, which can form tangles in the brain.
Gamma Oscillations Clean Up
“What this study does, in a very carefully designed and well-executed
way, is show that gamma oscillations, which we have known for a long
time are linked to cognitive function, play a critical role in the
capacity of the brain to clean up deposits,” says Alvaro Pascual-Leone, a
professor of neurology at Harvard Medical School who was not involved
in the research. “That’s remarkable and surprising, and it opens up the
exciting prospect of possible translation to application in humans.”
Tsai’s lab is now studying whether light can drive gamma
oscillations in brain regions beyond the visual cortex, and preliminary
data suggest that this is possible. They are also investigating whether
the reduction in amyloid plaques has any effects on the behavioral
symptoms of their Alzheimer’s mouse models, and whether this technique
could affect other neurological disorders that involve impaired gamma
oscillations.
Two Modes of Action
The researchers also performed studies to try to figure out how
gamma oscillations exert their effects. They found that after gamma
stimulation, the process for beta amyloid generation is less active.
Gamma oscillations also improved the brain’s ability to clear out beta
amyloid proteins, which is normally the job of immune cells known as
microglia.
“They take up toxic materials and cell debris, clean up the environment, and keep neurons healthy,” Tsai says.
In Alzheimer’s patients, microglia cells become very inflammatory
and secrete toxic chemicals that make other brain cells more sick.
However, when gamma oscillations were boosted in mice, their microglia
underwent morphological changes and became more active in clearing away
the beta amyloid proteins.
“The bottom line is, enhancing gamma oscillations in the brain can
do at least two things to reduced amyloid load. One is to reduce beta
amyloid production from neurons. And second is to enhance the clearance
of amyloids by microglia,” Tsai says.
The researchers also sequenced messenger RNA from the brains of the
treated mice and found that hundreds of genes were over- or
underexpressed, and they are now investigating the possible impact of
those variations on Alzheimer’s disease.
MORE INFORMATION:
The research was funded by the JPB Foundation, the Cameron Hayden Lord
Foundation, a Barbara J. Weedon Fellowship, the New York Stem Cell
Foundation Robertson Award, the National Institutes of Health, the
Belfer Neurodegeneration Consortium, and the Halis Family Foundation.
European Journal of Neurology — Gregson J, et al. | June 27, 2019
Because blood pressure (BP) is
thought to fall during the prodromal phase of dementia development,
researchers studied correlations by categories of time since BP
measurement (< 5 years, 5-10 years, > 10 years), and by dementia
subtypes. To explore the connection between BP and physician-diagnosed
dementia, Poisson regression models were used. The study sample
consisted of 2,593,629 individuals from the United Kingdom Clinical
Practice Research Database (aged ≥ 40 years) with a BP measurement
between 1992 and 2011, and no prior record of dementia. Investigators
found 65,618 cases of dementia during a median follow up of 8.2 years:
49,161 Alzheimer's, 13,816 vascular dementia, and 2,541 other subtypes.
In the short-term, elevated BP is linked to a reduced risk of dementia,
possibly due to reverse causation. BP's long-term dementia associations
are less marked and vary by subtype of dementia.
Multiple passes just means there is more time for that inflammatory action to occur. Bad conclusion, and the mentors and senior researchers didn't catch this and correct it? I take no prisoners in trying to get stroke to be fixed. Firings would occur under my watch.
Oops, I'm not playing by the polite rules of Dale Carnegie, 'How to Win Friends and Influence People'. Politeness
will never solve anything in stroke. I call them as I see them.
The
high prevalence of hyperintense acute reperfusion marker (HARM) seen
after endovascular therapy is suggestive of blood-brain barrier
disruption and hemorrhage risk and may be attributable to multiple
thrombectomy passes needed to achieve recanalization.
Methods—
Patients
with acute stroke were included if they were screened from January 2015
through February 2019, received an acute ischemic stroke diagnosis
involving the anterior circulation, treated with or without IV tPA
(intravenous tissue-type plasminogen activator), consented to the NINDS
Natural History Study, and imaged with a baseline magnetic resonance
imaging before receiving endovascular therapy. Consensus image reads for
HARM and hemorrhagic transformation were performed. Good clinical
outcome was defined as 0–2 using the latest available modified Rankin
Scale score.
Results—
Eighty
patients met all study criteria and were included in the analyses.
Median age was 65 years, 64% female, 51% black/African American, median
admit National Institutes of Health Stroke Scale=19, 56% treated with IV
tPA, and 84% achieved Thrombolysis in Cerebral Infarction score of
2b/3. Multiple-pass patients had significantly higher rates of severe
HARM at 24 hours (67% versus 29%; P=0.001), any hemorrhagic transformation (60% versus 36%; P=0.04) and poor clinical outcome (67% versus 36%; P=0.008). Only age (odds ratio, 1.1; 95% CI, 1.01–1.12; P=0.022)
and severe HARM at 24 hours post-endovascular therapy were
significantly associated with multiple passes (odds ratio, 7.2; 95% CI,
1.93–26.92; P=0.003).
Conclusions—
In
this exploratory study, multiple thrombectomy passes are independently
associated with a significant increase in blood-brain barrier disruption
detected at 24 hours. Patients with HARM post-endovascular therapy had a
>7-fold increase in the odds of having multiple- versus single-pass
thrombectomy.
Presented in part at the International Stroke Conference, Honolulu, HI, February 6–8, 2019.
Correspondence
to Marie Luby, PhD, Stroke Branch, National Institute of Neurological
Disorders and Stroke, National Institutes of Health, 10 Center Dr, Room
B1D-733, MSC 1063, Bethesda, MD 20892–1063. Email lubym@ninds.nih.gov
If they are using any information from the United States, that is worthless.
The supplements in the US have zero guarantee of purity or efficacy due to the fucking stupidity of the US Congress
passing the Dietary Supplement Health and
Education Act of 1994 (DSHEA).
Ginkgo Biloba is reputed to help with memory loss.
Photograph: Roger Tooth/The Guardian
Dietary supplements such as vitamins do nothing to boost brain health
and are simply a waste of money for healthy people, experts have said.
According to figures from the US, sales of so-called “memory
supplements” doubled between 2006 and 2015, reaching a value of $643m,
while more than a quarter of adults over the age of 50 in the US
regularly take supplements in an attempt to keep their brain in good
health.
But while bottles, packets and jars line the shelves of health food
shops – with claims that they help maintain brain function or mental
performance – a worldwide panel of experts says at present there is
little evidence that these supplements help healthy older people, and
that they could even pose a risk to health.
“There is no convincing evidence to recommend dietary supplements for
brain health in healthy older adults,” they write. “Supplements have
not been demonstrated to delay the onset of dementia, nor can they
prevent, treat or reverse Alzheimer’s disease or other neurological
diseases that cause dementia.”
However, the team note a lack of certain nutrients, such as vitamins
B9 and B12, appear to be linked to problems with cognitive function or
brain health, and that supplements might prove useful in people with deficiencies. About 20% of people over the age of 60 in the UK are thought to be lacking in vitamin B12.
But the experts stress it is important to consult a doctor before
starting any supplements, and that it is better to get nutrients from a
healthy diet.
At present, the team say, they cannot recommend healthy people take
supplements for brain health – although they stress further research is
needed. Their top recommendation is simple. “Save your money,” they
write. The report
by the Global Council on Brain Health looks at the evidence for a range
of supplements, including B vitamins, omega-3 fatty acids, vitamin D,
caffeine, coenzyme Q10 and ginkgo biloba.
The team found that few supplements which make claims about brain
health have actually been tested for their impact. Where studies do
exist they offer little or mixed evidence that supplements improve brain
function or prevent dementia.
“The big problem is that these things are
being marketed to people as if they have evidence,” said Linda Clare,
professor of clinical psychology of ageing and dementia at the
University of Exeter and a member of the team behind the report.
The team advise taking a sceptical view of such products, saying many
are marketed with exaggerated claims about their impact on mental
functions. They also stress that such pills, powders and capsules are
usually not subject to the same safety and efficacy tests as
medications.
However, Clare stressed the report only looked at the impact of
supplements on brain health. “The message is not that all supplements
are wrong for everything,” she said.
The report echoes recent findings by the Cochrane collaboration. Their study,
looking at evidence for effects of vitamin and mineral supplements on
cognitive function in over-40s, found no convincing effect for B
vitamins, selenium, zinc, vitamin E, omega-3, and only tentative
evidence of any benefit from long-term use of beta‐carotene or vitamin C
supplements.
Caroline Abrahams, charity director at Age UK, said of the new
report: “These eminent experts have concluded it doesn’t do any good to
take supplements to promote your brain health in later life so our
advice to older people is to save your money and spend it on a healthy
diet, full of delicious fruit and vegetables instead.”
David Smith, professor emeritus of pharmacology at the University of
Oxford, said that while the report was sensible, there were debates
about what constituted a vitamin deficiency – for example, low “normal”
levels might still have a negative impact on brain health. He also noted
that while consuming a Mediterranean diet
was good for the brain, as people got older they might not be as able
to absorb nutrients from food, while medications could potentially lead
to deficiencies. What’s more, plants contain no vitamin B12, so people
on a vegan diet should consider fortified foods or supplements.
Smith added that while the report called for more high-quality
research to improve the evidence base, there was a significant stumbling
block. “The problem is that the authorities and drug companies seem to
be reluctant to support such trials on vitamins, partly because there is
no obvious financial benefit and because no patents can be filed,” he
said.
Experts say there are many other steps individuals can take to keep
sharp as they age – including not smoking, sleeping well, exercising and
keeping socially engaged and mentally stimulated.
Prof Gill Livingston of University College London added that people
should also get their blood pressure and hearing checked to prevent
dementia. “Drugs for high blood pressure are currently the only known
effective preventive medication for dementia,” she said.
I'm focusing on the line, neuroprotection fell out of favor. Would it have fallen out of favor if it was properly referred to as the neuronal cascade of death?
Survivors in charge would never have let it fall out of favor. Will you all step aside and let survivors run this the proper way? Leading to 100% recovery.
While
advances in stroke generally continue to accelerate in terms of
prevention, acute intervention, and recovery, the speed at which these
changes are occurring is quite impressive. The introduction of
thrombolysis as the first major acute intervention in acute ischemic
stroke spreads at a fairly modest pace around the world, although it
accelerated in later years as its efficacy became more clearly
established with pooled analysis of existing trials and extension of the
therapeutic stroke window out to 4.5 h. There was undoubtedly some
reticence on the part of a smaller cohort of emergency physicians in
some parts of the world to embrace thrombolysis as a stroke therapy, but
this now has been dissipated by the tsunami of thrombectomy. The
greater efficacy of thrombectomy with numbers needed to treat as low as 3
has led to its extraordinarily rapid uptake around the globe,
particularly in the developed world. This was partly assisted by the
health care systems, particularly involving stroke units, which provided
fertile ground for the next therapeutic wave, certainly further
adjustments in health care services have been required, and more work in
this area needs to be done but not near the magnitude of change that
was initially required after thrombolysis. Of course, change in
low–middle income countries (LMICs) is taking a proportionately longer
time to install these services.
A manifestation of the dynamics of
these developments has been the changing emphasis of the longstanding
14th International Symposium on Thrombolysis, Thrombectomy and Acute
Stroke Therapy: Proceedings and Summary of Discussions. This is usually
held as a satellite to world stroke meetings since its inception. In
earlier meetings, thrombolysis was the main focus, and then
neuroprotection was added but later fell out of favor. The current
meeting, held in Houston recently and reported in this edition, has a
strong emphasis on thrombectomy and thrombolysis. It has been a driver
of intellectual thought on acute therapy.
In keeping with our
acute intervention theme, we also have a meta-analysis on glial
fibrillary acidic protein as a biomarker for the presence of
intracerebral hemorrhage. This represents one of a number of ongoing
attempts to enable a distinction to be made between hemorrhagic and
ischemic stroke, which will be of particular relevance in LMICs where
imaging may not be readily available. Other attempts to improve
pre-hospital diagnosis of stroke also appear in this edition with
pre-hospital stroke scores to identify stroke mimics and also better
algorithms for emergency service call centers.
Such energy
focussed on the various aspects of stroke management throughout the
continuum of care seems to be producing tangible benefits. We are
delighted to be a vehicle to help bring this information to our global
community.
This needs to change from guideline development to protocol development. Guidelines are lazy and not terribly useful in getting to 100% recovery. Survivors need certainty and guidelines don't provide that. Stress, anxiety and depression are a result of not having protocols. This change won't occur until we get survivors in charge. Firings should start as soon as possible.
The 2019 update of the Canadian Stroke Best Practice Recommendations (CSBPR) for Mood, Cognition and Fatigue following Stroke
is a comprehensive set of evidence-based guidelines addressing three
important issues that can negatively impact the lives of people who have
had a stroke. These include post-stroke depression and anxiety,
vascular cognitive impairment, and post-stroke fatigue. Following
stroke, approximately 20% to 50% of all persons may be affected by at
least one of these conditions. There may also be overlap between
conditions, particularly fatigue and depression. If not recognized and
treated in a timely matter, these conditions can lead to worse long-term
outcomes. The theme of this edition of the CSBPR is Partnerships and Collaborations,
which stresses the importance of integration and coordination across
the healthcare system to ensure timely and seamless care to optimize
recovery and outcomes. Accordingly, these recommendations place strong
emphasis on the importance of timely screening and assessments, and
timely and adequate initiation of treatment across care settings.
Ideally, when screening is suggestive of a mood or cognition issue,
patients and families should be referred for in-depth assessment by
healthcare providers with expertise in these areas. As the complexity of
patients treated for stroke increases, continuity of care and strong
communication among healthcare professionals, and between members of the
healthcare team and the patient and their family is an even bigger
imperative, as stressed throughout the recommendations, as they are
critical elements to ensure smooth transitions from acute care to active
rehabilitation and reintegration into their community.
Globally, stroke is the second most common cause of all deaths (11.8%), behind ischemic heart disease at 14.8%.1
In Canada, every year, approximately 62,000 people with stroke and
transient ischemic attack (TIA) are treated in Canadian hospitals,
representing one patient every 9 min.2
Not counted in this statistic are the estimated nine silent strokes
that occur for each symptomatic stroke, often resulting in subtle mood
and cognitive changes.3
With advancements in acute stroke care interventions and rapid systems
response, mortality from stroke is declining. While these achievements
are to be celebrated, stroke remains a leading cause of adult
disability, with over 400,000 people living with its effects.4
Access to inpatient rehabilitation varies across regions, with only 19%
of people accessing inpatient rehabilitation following an acute stroke
inpatient stay. There are also gaps in availability of specialized
services outside large urban centers.
Common consequences of
stroke, including post-stroke depression (PSD) and anxiety, vascular
cognitive impairment (VCI), and post-stroke fatigue (PSF), create
challenges that may impede recovery and lead to poor functional outcomes
and decreased quality of life. Following stroke, between 20% and 50% of
all persons may be affected by at least one of these conditions.5–7
There can be overlap in the occurrence of these conditions, increasing
the complexity of diagnosis and appropriate management. Fatigue and
depressive symptoms have been shown to co-exist in up to 30% of stroke
survivors, which in turn may be associated with cognitive and mobility
impairments.8
The overall prevalence of depression in persons with mild cognitive
impairment (MCI) was 32% in a meta-analysis including the results of 57
studies.9 Persons with depression may progress more quickly from MCI to dementia.10 These conditions all have the potential to delay or impede recovery, which may lead to worse long-term outcomes.11–13
Unfortunately, these conditions may not be obvious to the person who
experienced a stroke, their healthcare providers or their informal
caregivers, especially if symptoms are mild or manifest slowly and
progressively, or are present only later in the recovery process, when
care becomes more fragmented in the community. Furthermore, recent
reports on the quality of stroke services across Canada have shown that
screening and monitoring of patients for PSD, fatigue, and vascular
cognitive functioning issues are completed in just over half of people
seen in stroke prevention clinics following stroke or TIA.14
As a result, these conditions may not be recognized and treated in a
timely manner, leaving patients and their families overwhelmed and lost
as they try to navigate the healthcare system, and underscoring the need
for a standardized system of care for addressing these conditions
across the continuum.15
The
2019 update of the Canadian Stroke Best Practice Recommendations
(CSBPR): Mood, Cognition and Fatigue following Stroke is a comprehensive
summary of current evidence-based recommendations, focusing on the
management of people who have already had an initial stroke or TIA. The
theme of this edition of the CSBPR is Partnerships and Collaborations,
which stresses the importance of integration and coordination across
the healthcare system to ensure timely and seamless care of stroke
patients to optimize recovery and outcomes. The importance of a
coordinated and organized multidisciplinary approach to guide screening,
assessment, and management decisions are emphasized throughout these
guidelines, which are appropriate for use by clinicians who care for
people who have experienced a stroke and their families, across multiple
settings.
What’s new in 2019?
In
areas where insufficient evidence exists, a new section, entitled
clinical considerations has been added to each section, representing
recommendations based on weaker evidence and/or expert consensus-based
practices. In the depression section, new literature has been
incorporated which suggests that prophylactic antidepressant medication
can be effective in some stroke patients. There is a new, novel
therapeutic agent, actovegin, which enhances oxidative metabolism in the
brain and may help in the recovery of cognitive function following
ischemic stroke. While it is not used currently in clinical practice, it
may become more widely used in the future. There is also an updated
comparison table of assessment tools for screening for VCI and updated
information on the management of PSF.
Guideline development methodology
The Canadian Stroke Best Practice Recommendations
development and update process follows a rigorous framework adapted
from the Practice Guideline Evaluation and Adaptation Cycle.16,17 The methodology has been used in previously published updates18,19 and can be found on our Canadian Stroke Best Practices website at www.strokebestpractices.ca.
An interdisciplinary group of experts in the areas of depression,
anxiety, cognition, and fatigue were convened and participated in
reviewing, drafting, and revising all recommendation statements.
Selected members of the group, considered to be experts in their fields,
have conducted clinical trials on the topics addressed in this module
and have extensive publication records. The writing group included
stroke neurologists, a geriatric psychiatrist, a clinical
pharmacologist, neuropsychologists, occupational therapists, a
speech-language pathologist, family physician, nurses, people who have
experienced a stroke and evidence-based methodology experts. This
interdisciplinary approach, which ensured that all perspectives were
considered in the development of the recommendations, mitigated the risk
of potential or real conflicts of interest from individual members.
A systematic literature search was conducted by experienced personnel to identify evidence for each topic area addressed in the Mood, Cognition and Fatigue following Stroke
module. The literature for this module was updated up to February 2019.
The writing group was provided with comprehensive evidence tables that
included summaries of all high-quality studies identified through the
literature searches (evidence tables are available at www.strokebestpractices.ca).
Systematic reviews, meta-analyses, randomized controlled trials, and
observational studies were included, where available. The writing group
discussed and debated the quality and value of the evidence and, through
consensus, developed a set of proposed recommendations. Through their
discussions, additional research may have been identified and included
in the evidence tables if consensus on the value of the research was
achieved.
All recommendations were assigned a level of evidence ranging from A to C, according to the criteria defined in Table 1.
When developing and including “C-Level” recommendations, consensus was
obtained among the writing group and validated through the internal and
external review process. This level of evidence was used cautiously, and
only when there was a lack of stronger evidence for topics considered
important system drivers for stroke care (e.g. issues related to
screening and assessment). In some sections, the expert writing group
felt there was additional information that should be included. Since
these statements did not meet the criteria to be stated as
recommendations, they were included under the term, clinical considerations, with the goal of providing additional guidance or clarity in the absence of evidence.
Table 1. Summary of criteria for levels of evidence reported in the Canadian Best Practice Recommendations for Stroke Care (update 2019)
Table 1. Summary of criteria for levels of evidence reported in the Canadian Best Practice Recommendations for Stroke Care (update 2019)
After
a draft set of recommendations had been developed, they underwent an
internal review conducted by the Canadian Stroke Best Practices and
Quality Advisory Committee, then were sent for external review to
several Canadian and international experts who were not involved in any
aspects of the guideline development. All feedback received was given
careful consideration during the editing process. All recommendations
are also accompanied by five additional supporting sections devoted to:
the rationale (i.e. the justification for the inclusion of the selected
topics), system implication (to ensure the structural elements and
resources are available to achieve recommended levels of care),
performance measures (to monitor care delivery and patient outcomes), a
list of implementation resources, and a summary of the evidence on which
the recommendations were based. Brief summaries of current research
evidence are provided at the beginning of each section below. More
detailed evidence summaries and links to all evidence tables, and
additional knowledge translation information for the recommendations
included in this publication can be found at: http://www.strokebestpractices.ca. For a more detailed description of the methodology on the development and dissemination of the Canadian Stroke Best Practice Recommendations please refer to the Canadian Stroke Best Practice Recommendations Overview and Methodology documentation available on the Canadian stroke best practices website at: http://www.strokebestpractices.ca.
Recommendations Section 1: Mood and stroke
Post
stroke depression occurs frequently. One of the most current and
comprehensive estimates, obtained from a systematic review that included
the results of 61 prospective studies, suggests that approximately 30%
of all stroke survivors experience depressive symptoms at some point
following the event.5
The prevalence of depressive symptoms among stroke survivors is greater
than that in the general population. The estimate obtained from one
population-based study20
indicated that over a two-year period, the development of new-onset
depression was over three times greater (25.4% vs. 7.8%; adj HR = 4.09,
95% confidence interval (CI) 4.00–4.18) in persons recovering from
stroke compared to a large, age and sex-match community-based sample.
Risk factors for the development of PSD include increasing age, living
alone, high levels of comorbidity, a history of depression, female
gender, physical disability (modified Rankin Scale score >2 at
discharge from hospital), increased initial stroke severity, cognitive
impairment, and prior history of stroke.13,20–22 Depression has also been associated with poorer functional outcomes and higher mortality.13,23
Since the frequency of depression is highest during the first year following stroke,5
episodic screening should be conducted during this period. Screening
can be performed during the acute inpatient stay, at the point of
transition to, or during inpatient rehabilitation, upon discharge to the
community and during routine health assessments. Although screening for
depression has been shown to be feasible for most patients, it may not
be in a sizable minority due to cognitive deficits or unresponsiveness
during the early period following stroke. Karamchandani et al.24
reported that while 70% of patients were eligible for depression
screening prior to hospital discharge or transfer to another service,
the remaining 30% of patients were not, due to aphasia, other medical
condition, hospice/comfort measures, or prolonged intubation. Swartz
et al.11
describes the feasibility of using the two-item version of the Patient
Health Questionnaire during routine clinical practice for 1500
outpatients attending a stroke prevention clinic. All patients were able
to complete the screen, 89% of whom did so in less than 5 min. While
many previously validated screening tools exist, those with the highest
sensitivities identified from a recent meta-analysis include the 20-item
Center of Epidemiological Studies-Depression Scale, the 21-item
Hamilton Depression Rating Scale, and the 9-item Patient Health
Questionnaire.25
The
use of antidepressants is the mainstay of treatment for depression.
Once diagnosed, use of antidepressants has been associated with a
reduction of depressive symptomatology. Xu et al.26
included 11 randomized controlled trials in a meta-analysis of patients
with a clinical diagnosis of PSD and reported that antidepressant
treatment was associated with a significant reduction in depression
scores (standardized mean difference = −0.96, 95% CI −1.41 to −0.51,
p < 0.0001) and better response to treatment (risk ratio = 1.36, 95%
CI 1.01–1.83, p = 0.04). Similarly, a Cochrane review27
including the results from 12 RCTs reported the odds of remission of
depression (i.e. a reduction of ≥50% in depression scale scores) were
significantly higher with pharmacotherapy, although many adverse events
were reported. Most of the agents evaluated in these reviews were
selective serotonin reuptake inhibitors and, to a lesser extent,
tricyclic antidepressants. A longer duration of treatment has been shown
to be effective. In one systematic review, Chen et al.28
observed an almost perfect inverse linear relationship between length
of treatment and decrease in depression rating scale scores (Spearman’s
rho = −0.93, p = 0.001). The benefit of antidepressants to improve
functional recovery and reduce dependency in persons following stroke is
uncertain, given the conflicting results of the FLAME trial,29
which reported improved functional outcome following 90 days of
treatment with 20 mg of fluoxetine (vs. placebo), and the recent FOCUS
trial,30
which reported no differences in dependency between groups (20 mg
fluoxetine vs. placebo) at six or 12 months. The use of antidepressants
has been associated with reductions in emotional lability,31
a common consequence of stroke as well as the development of PSD. In
pooled analysis, based on 776 observations, the risk for development of
PSD was significantly reduced with the use of prophylactic
pharmacotherapy (odds ratio (OR) = 0.34, 95% 0.22–0.53, p < 0.001).32,33
Non-pharmacological
interventions for the treatment of PSD include different forms of
psychotherapy, physical activity, non-invasive brain stimulation, and
acupuncture. While psychotherapy (including problem-solving therapy,
cognitive behavioral therapy, and motivational interviewing) is probably
one of the most commonly used strategies, it has not been shown to be
an effective treatment for depression in person recovering from stroke
when used in isolation27; however, these same techniques may be effective when used in combination with pharmacotherapy.34 Behavioral therapy was shown to be effective for the treatment of PSD in persons with aphasia.35
Although not widely used in clinical practice, acupuncture has been
shown to be effective in the treatment of PSD. In a meta-analysis
including the results of 15 RCTs,36
treatment with acupuncture was associated with improved odds of
recovery/remission compared with pharmacotherapy (OR = 1.48, 95% CI
1.10–1.97). Non-invasive brain stimulation, using either repetitive
transcranial magnetic stimulation or transcranial direct current
stimulation (tDCS), is another example of a non-traditional treatment
that has been shown to improve symptoms of depression.37,38
Physical activity was also associated with a small, but significant
reduction in depression scores in a meta-analysis that pooled the
results of 13 RCTs (SMD = −0.13, 95% CI −0.26 to −0.01, p = 0.03).39
