Deans' stroke musings

Changing stroke rehab and research worldwide now.Time is Brain!Just think of all the trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 493 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It's quite disgusting that this information is not available from every stroke association and doctors group.
My back ground story is here:

Thursday, March 16, 2017

Oxford University to launch study on medical benefits of marijuana

Hopefully some stroke survivor has contacts there and can get stroke rehab on the study list.

My 13 reasons for marijuana use post-stroke.  

But don't listen to me, I have absolutely no medical training.

Researchers at Oxford University are to undertake a £10 million study on the medical benefits of marijuana in treating pain, cancer and inflammatory diseases.

It follows calls from some MPs for a law to allow medical use of cannabis, with polls suggesting  58 per cent of people would back such a move.
In recent years, studies have increasingly supported the medical value of cannabis in treating such conditions as multiple sclerosis, epilepsy and arthritis, and for dealing with nerve pain.

The study, entitled the Cannabis Research Plan, is to be a partnership between Oxford University and venture capital company Kingsley Capital Partners, who are investing £10 million to create a global centre of excellence in cannabinoid research.
Prof Ahmed Ahmed of Oxford's Nuffield Department of Obstetrics and Gynaecology, said existing studies were beginning to produce exciting findings which could result in new treatments. “This field holds great promise for developing novel therapeutic opportunities for cancer patients,” he said.
The study has received celebrity backing from actor Sir Patrick Stewart, who uses marijuana to treat the symptoms of his ortho-arthritis. He told The Daily Telegraph: “Two years ago, in Los Angeles I was examined by a doctor and given a note which gave me legal permission to purchase, from a registered outlet, cannabis-based products, which I was advised might help the ortho-arthritis in both my hands.”

Regular use of an ointment and chewy bar had allowed him to sleep at night, while spraying his hands during the day had brought back mobility, he said, enabling him to make fists.
“As a result of this experience, I enthusiastically support the Oxford University Cannabis Research Plan,” he said.
The star of the X-Men and Star Trek films hopes the research will help him and millions of others. “This is an important step forward for Britain in a field of research that has, for too long, been held back by prejudice, fear and ignorance,” he said.
Currently neither the Conservatives nor Labour officially support legalising cannabis for medical use. Both the Green Party and the Liberal Democrats have called for legalising its medical use for some time.
Sativex, a prescription-only drug used by multiple sclerosis patients, is the only licensed cannabis-based product in the country and is given to help ease muscle spasms. However, it is non-psychoactive and does not cause a high.
To date, NHS bodies have rejected its use, saying it is too costly to justify.

Trump's First Budget Proposes Big Changes for Science Research

If our fucking failures of stroke associations haven't already realized it, the complete model of stroke research is likely upended. It is quite simple to execute and solve all the fucking problems in stroke.  Yes these are BHAGs(Big Hairy Audacious Goals) but so what?
1.  Create a stroke strategy that solves all the problems in stroke and leads to 100% recovery for all..
2. Creates RFPs to researchers to answer the questions in the strategy in a defined order.
3. Get foundation grants to pay for such research. Specific research goals are much more likely to be funded.
4. Work the strategy until all the fucking problems in stroke are solved and every stroke survivor gets to 100% recovery.
5. If that is not your goal get the hell out of the way for those leaders willing to try and succeed.

Tree clearing

Using my 13 inch pruning saw it took 3 evenings of 20 minutes each to get this cleared. The trail only goes 30 yards beyond this point so pretty much worthless to do, except I felt compelled. The angled branch I was able to roll off the connecting piece on the tree, crashing it to the ground.

Brain is 10 times more active than previously measured, UCLA researchers find

Do you really think your doctor has any clue how to get you 100% recovered when we currently know jackshit about how the brain works?  I bet your doctor and stroke hospital are not collaborating with any researchers to understand and fix the brain. If they are not, the complete stroke department and all the leaders in the stroke hospital need to be fired.
A new UCLA study could change scientists' understanding of how the brain works - and could lead to new approaches for treating neurological disorders and for developing computers that "think" more like humans.
The research focused on the structure and function of dendrites, which are components of neurons, the nerve cells in the brain. Neurons are large, tree-like structures made up of a body, the soma, with numerous branches called dendrites extending outward. Somas generate brief electrical pulses called "spikes" in order to connect and communicate with each other. Scientists had generally believed that the somatic spikes activate the dendrites, which passively send currents to other neurons' somas, but this had never been directly tested before. This process is the basis for how memories are formed and stored.
Scientists have believed that this was dendrites' primary role.
But the UCLA team discovered that dendrites are not just passive conduits. Their research showed that dendrites are electrically active in animals that are moving around freely, generating nearly 10 times more spikes than somas. The finding challenges the long-held belief that spikes in the soma are the primary way in which perception, learning and memory formation occur.
"Dendrites make up more than 90 percent of neural tissue," said UCLA neurophysicist Mayank Mehta, the study's senior author. "Knowing they are much more active than the soma fundamentally changes the nature of our understanding of how the brain computes information. It may pave the way for understanding and treating neurological disorders, and for developing brain-like computers."
The research is reported in the journal Science.
Scientists have generally believed that dendrites meekly sent currents they received from the cell's synapse (the junction between two neurons) to the soma, which in turn generated an electrical impulse. Those short electrical bursts, known as somatic spikes, were thought to be at the heart of neural computation and learning. But the new study demonstrated that dendrites generate their own spikes 10 times more often than the somas.
The researchers also found that dendrites generate large fluctuations in voltage in addition to the spikes; the spikes are binary, all-or-nothing events. The somas generated only all-or-nothing spikes, much like digital computers do. In addition to producing similar spikes, the dendrites also generated large, slowly varying voltages that were even bigger than the spikes, which suggests that the dendrites execute analog computation.
"We found that dendrites are hybrids that do both analog and digital computations, which are therefore fundamentally different from purely digital computers, but somewhat similar to quantum computers that are analog," said Mehta, a UCLA professor of physics and astronomy, of neurology and of neurobiology. "A fundamental belief in neuroscience has been that neurons are digital devices. They either generate a spike or not. These results show that the dendrites do not behave purely like a digital device. Dendrites do generate digital, all-or-none spikes, but they also show large analog fluctuations that are not all or none. This is a major departure from what neuroscientists have believed for about 60 years."
Because the dendrites are nearly 100 times larger in volume than the neuronal centers, Mehta said, the large number of dendritic spikes taking place could mean that the brain has more than 100 times the computational capacity than was previously thought.
Recent studies in brain slices showed that dendrites can generate spikes. But it was neither clear that this could happen during natural behavior, nor how often. Measuring dendrites' electrical activity during natural behavior has long been a challenge because they're so delicate: In studies with laboratory rats, scientists have found that placing electrodes in the dendrites themselves while the animals were moving actually killed those cells. But the UCLA team developed a new technique that involves placing the electrodes near, rather than in, the dendrites.
Using that approach, the scientists measured dendrites' activity for up to four days in rats that were allowed to move freely within a large maze. Taking measurements from the posterior parietal cortex, the part of the brain that plays a key role in movement planning, the researchers found far more activity in the dendrites than in the somas - approximately five times as many spikes while the rats were sleeping, and up to 10 times as many when they were exploring.
"Many prior models assume that learning occurs when the cell bodies of two neurons are active at the same time," said Jason Moore, a UCLA postdoctoral researcher and the study's first author. "Our findings indicate that learning may take place when the input neuron is active at the same time that a dendrite is active - and it could be that different parts of dendrites will be active at different times, which would suggest a lot more flexibility in how learning can occur within a single neuron."
Looking at the soma to understand how the brain works has provided a framework for numerous medical and scientific questions - from diagnosing and treating diseases to how to build computers. But, Mehta said, that framework was based on the understanding that the cell body makes the decisions, and that the process is digital.
"What we found indicates that such decisions are made in the dendrites far more often than in the cell body, and that such computations are not just digital, but also analog," Mehta said. "Due to technological difficulties, research in brain function has largely focused on the cell body. But we have discovered the secret lives of neurons, especially in the extensive neuronal branches. Our results substantially change our understanding of how neurons compute."
The study's other authors are Pascal Ravassard, David Ho, Lavanya Archarya, Ashley Kees and Cliff Vuong, all of UCLA. Funding was provided by the University of California.
Article: Dynamics of cortical dendritic membrane potential and spikes in freely behaving rats, Jason J. Moore, Pascal M. Ravassard, David Ho, Lavanya Acharya, Ashley L. Kees, Cliff Vuong, Mayank R. Mehta, Science, doi: 10.1126/science.aaj1497, published 9 March 2017.

Caffeine: How much is too much?

Where is your doctors' coffee protocol? I've only written 125 posts on coffee, most of them on the benefits. Does your doctor not read any research or employ an analyst to summarize research for them? Such incompetency should require a call to the president and board of directors to see how far up the rot goes. Sometimes you need to amputate before the rot kills the patient.

So the question to be answered. How much coffee should we be drinking per body weight/sex? Specifics, not this generalized crap.
Nothing reported on this.

Coffee linked with increased cardiovascular risk in young adults(18-45) with mild hypertension

By Mayo Clinic Staff
If you rely on caffeine to wake you up and keep you going, you aren't alone. Caffeine is used daily by millions of people to increase wakefulness, alleviate fatigue, and improve concentration and focus.

How much is too much?

Up to 400 milligrams (mg) of caffeine a day appears to be safe for most healthy adults. That's roughly the amount of caffeine in four cups of brewed coffee, 10 cans of cola or two "energy shot" drinks. Keep in mind that the actual caffeine content in beverages varies widely, especially among energy drinks.
Although caffeine use may be safe for adults, it's not a good idea for children. Adolescents should limit caffeine consumption. Avoid mixing caffeine with other substances, such as alcohol.
Even among adults, heavy caffeine use can cause unpleasant side effects. And caffeine may not be a good choice for people who are highly sensitive to its effects or who take certain medications.
Women who are pregnant or who are trying to become pregnant and those who are breastfeeding should talk with their doctors about limiting caffeine use.
Read on to see if you may need to curb your caffeine routine.

You drink more than 4 cups of coffee a day

You may want to cut back if you're drinking more than 4 cups of caffeinated coffee a day (or the equivalent) and you're experiencing side effects such as:
  • Migraine headache
  • Insomnia
  • Nervousness
  • Irritability
  • Restlessness
  • Frequent urination or inability to control urination
  • Stomach upset
  • Fast heartbeat
  • Muscle tremors

Even a little makes you jittery

Some people are more sensitive to caffeine than are others. If you're susceptible to the effects of caffeine, just small amounts — even one cup of coffee or tea — may prompt unwanted effects, such as restlessness and sleep problems.
How you react to caffeine may be determined in part by how much caffeine you're used to drinking. People who don't regularly drink caffeine tend to be more sensitive to its negative effects. Other factors may include genetics, body mass, age, medication use and health conditions, such as anxiety disorders.

You're not getting enough sleep

Most adults need seven to eight hours of sleep each night. But caffeine, even in the afternoon, can interfere with this much-needed sleep.
Chronically losing sleep — whether it's from work, travel, stress or too much caffeine — results in sleep deprivation. Sleep loss is cumulative, and even small nightly decreases can add up and disturb your daytime alertness and performance.
Using caffeine to mask sleep deprivation can create an unwelcome cycle. For example, you may drink caffeinated beverages because you have trouble staying awake during the day. But the caffeine keeps you from falling asleep at night, shortening the length of time you sleep.

You're taking medications or supplements

Certain medications and herbal supplements may interact with caffeine. Examples include:
  • Ephedrine. Mixing caffeine with this medication — which is used in decongestants — might increase your risk of high blood pressure, heart attack, stroke or seizure.
  • Theophylline (Theo-24, Elixophyllin, others). This medication, used to open up bronchial airways, tends to have some caffeine-like effects. So taking it with caffeine might increase the adverse effects of caffeine, such as nausea and heart palpitations.
  • Echinacea. This herbal supplement, which is sometimes used to prevent colds or other infections, may increase the concentration of caffeine in your blood and may increase caffeine's unpleasant effects.
Talk to your doctor or pharmacist about whether caffeine might affect your medications.

Curbing your caffeine habit

Whether it's for one of the reasons above — or because you want to trim your spending on coffee drinks — cutting back on caffeine can be challenging. An abrupt decrease in caffeine may cause withdrawal symptoms, such as headaches, fatigue, irritability and difficulty focusing on tasks. Fortunately, these symptoms are usually mild and resolve after a few days.
To change your caffeine habit, try these tips:
  • Keep tabs. Start paying attention to how much caffeine you're getting from foods and beverages, including energy drinks. Read labels carefully. But remember that your estimate may be a little low because some foods or drinks that contain caffeine don't list it.
  • Cut back gradually. For example, drink one fewer can of soda or drink a smaller cup of coffee each day. Or avoid drinking caffeinated beverages late in the day. This will help your body get used to the lower levels of caffeine and lessen potential withdrawal effects.
  • Go decaf. Most decaffeinated beverages look and taste the same as their caffeinated counterparts.
  • Shorten the brew time or go herbal. When making tea, brew it for less time. This cuts down on its caffeine content. Or choose herbal teas that don't have caffeine.
  • Check the bottle. Some over-the-counter pain relievers contain caffeine — as much as 130 mg of caffeine in one dose. Look for caffeine-free pain relievers instead.

The bottom line

If you're like most adults, caffeine is a part of your daily routine. And most often it doesn't pose a health problem. But be mindful of those situations in which you need to curtail your caffeine habit.

Pot Use Tied to Higher Odds for Stroke, Heart Failure

That is quite a jump from concluding that pot use as specified in the question is tied to heart attacks and stroke.  I tried marijuana in college and nothing about my use of it then led in any way to my stroke. I also drank lots of beer in college and that could just as easily be pointed to as a risk factor for stroke and heart attack.  False association but good for big pharma to demonize marijuana. I will try it for rehab after my next stroke. This is total biased research, they had an agenda to write on and they manufactured the conclusions.

My 13 reasons for marijuana use post-stroke.  

But don't listen to me, I have absolutely no medical training.
New research analyzing millions of U.S. medical records suggests that marijuana use raises an adult's risk of stroke and heart failure.
The study couldn't prove cause-and-effect, but the researchers said they tried to account for other heart risk factors.
"Even when we corrected for known risk factors, we still found a higher rate of both stroke and heart failure in these patients," explained lead researcher Dr. Aditi Kalla, a cardiologist at Einstein Medical Center in Philadelphia.
"That leads us to believe that there is something else going on besides just obesity or diet-related cardiovascular side effects," Kalla said in a news release from the American College of Cardiology (ACC).
Her team is slated to present its findings March 18 at the ACC's annual meeting, in Washington, D.C.
In the study, Kalla's group looked at 20 million health records of patients aged 18 to 55 who were discharged from one of more than a thousand hospitals across the United States in 2009 and 2010.
Of those patients, 1.5 percent said they'd used marijuana.
Such use was associated with a much higher risk for stroke, heart failure, coronary artery disease and sudden cardiac death. Pot use was also tied to common heart disease risk factors such as obesity, high blood pressure, smoking and drinking, the researchers said.
After adjusting for those risk factors, the researchers concluded that marijuana use was independently associated with a 26 percent increased risk of stroke and a 10 percent increased risk of heart failure.
"More research will be needed to understand the [reasons] behind this effect," Kalla said.
Not everyone agreed the findings are cause for alarm, however.
Paul Armentaro is deputy director of NORML, a marijuana advocacy group. He called the increase in heart risk, "a relatively nominal one," and said the study "is inconsistent with the findings of several other longitudinal studies finding that those who consume cannabis, but not tobacco, suffer no greater likelihood of adverse events compared to those with no history of use."
NORML agrees that certain groups -- adolescents, pregnant or nursing mothers, people with a history of psychiatric illness, or those with a prior history of heart disease -- may want to avoid marijuana due to the potential effects on health.
But others may want to talk the issue over with their doctors. "As with any medication, patients should consult thoroughly with their physician before deciding whether the medical use of cannabis is safe and appropriate," Armentaro said. (What the hell good would that do, your doctor knows nothing about benefits of marijuana?)
Study author Kalla noted that medical or recreational marijuana use is now legal in more than half of U.S. states -- so a better understanding of its health effects is needed.
"Like all other drugs, whether they're prescribed or not prescribed, we want to know the effects and side effects of this drug," Kalla said. "It's important for physicians to know these effects so we can better educate patients, such as those who are inquiring about the safety of cannabis or even asking for a prescription for cannabis."
Two heart specialists agreed.
The new study "suggests that marijuana may not be as safe as proponents for its legalization claim,"(bullshit! the study does no such thing) said Dr. Andrew Rogove, who directs stroke care at Southside Hospital in Bay Shore, N.Y. He believes that "further studies need to be performed to elucidate how marijuana use can increase risk for stroke and heart failure and if any particular way that it is used confers a higher risk."
Dr. Shazia Alam directs inpatient stroke services at Winthrop-University Hospital, in Mineola, N.Y. She believes there's a growing number of patients of all ages with a history of marijuana use.
"As more of our patients will be on marijuana in the near future given the legalization trend, this study reminds us how important it is to ask about marijuana use early on and inform them of any potential consequences," she said.
"Moreover, we have been seeing increased strokes in the younger population, therefore routinely inquiring about marijuana use may become an integral part in stroke prevention," Alam added.
Because these findings are to be presented at a medical meeting, they should be considered preliminary until published in a peer-reviewed journal.
More information
The U.S. National Institute on Drug Abuse has more about marijuana. (This proves the bias.)
-- Robert Preidt SOURCES: Shazia Alam, D.O., director, inpatient neurology and stroke services, Winthrop-University Hospital, Mineola, NY; Andrew Rogove, M.D., medical director, stroke, Southside Hospital, Bay Shore, N.Y.; Paul Armentaro, deputy director, NORML; American College of Cardiology, news release, March 9, 2017

“Off-the-charts dangerous”: Sham stem cell trial at Florida clinic blinds three women

Be careful out there. I have seen nothing to prove stem cell therapy for brains work. Gordie Howe anecdotes prove nothing.

The problems that can occur:

Donor-derived brain tumor following neural stem cell transplantation in an ataxia telangiectasia patient.


He went abroad for stem cell treatment. Now he’s a cautionary tale. Stroke patient Jim Gass

Stem cell propagation fuels cancer risk in different organs

New Blood Test Could Help Prevent Heart Attack and Stroke

Wrong, it doesn't prevent, it only identifies a risk factor.
Scientists can tell by your blood whether you have cancer cells, how well your organs are functioning, and if they've been affected by cancer. Now there’s a new blood test that could help prevent heart attacks and strokes.
Jeff Meeusen, Ph.D., developed the test at the Mayo Clinic in Rochester, Minnesota. Meeusen told VOA in a Skype interview that the test will determine who’s at risk for a heart attack or stroke, "and it seems to have a chance to determine who’s at risk, even accounting for current gold standard tests like LDL (low-density lipoprotein) cholesterol." LDL cholesterol is considered the "bad" cholesterol because it becomes part of plaque, the waxy stuff that can clog arteries.
The test measures the amount of ceramides in the blood. Ceramides are waxy molecules strongly linked to cardiovascular disease. They are similar to cholesterol, but unlike cholesterol, they are biologically active.
Meeusen explained that when we start to have cardiovascular risk factors, the ceramide levels build up and then they can promote things like the LDL cholesterol crossing into the vascular wall. Once it’s there, he said, ceramides develop atheroscopic plaque, which causes hardening of the arteries.
"Even if you have a very low LDL cholesterol, this ceramide test is able to identify who is going to be at risk for developing a heart attack or stroke later in life," Meeusen said. Meeusen is a clinical chemist and co‑director of Cardiovascular Laboratory Medicine at the Mayo Clinic.
The test could be used to help patients who have progressing coronary artery disease as well as to find out who is at risk for developing coronary artery disease.
Our physicians are really embracing this new test," Meesen said. "There’s been a need for tests that can help identify those people that are at higher risk, and they’re using this test among individuals that would otherwise seem to be at target, on track. They have good cholesterol. They don’t have too many other risk factors. And yet, if you have an elevated ceramide score, being able to prescribe a statin, or encourage that patient to exercise and diet, is going to prevent these events in the long run."
Meeusen said the test provides an incentive to patients to take better care of their health. What's more, the test is available to doctors and their patients outside the Mayo Clinic hospital network.

Wednesday, March 15, 2017

Researchers Explore Multimodal Technology for Assessing Stroke Symptoms

Still looking at the effects of the stroke rather than the actual damage in the brain.  The same effect, not able to move arm could have 9 different causes. Don't tell me all of those causes would have the same treatment protocol.
1. Penumbra damage to the motor cortex.
2. Dead brain in the motor cortex.
3. Penumbra damage in the pre-motor cortex.
4. Dead brain in the pre-motor cortex.
5. Penumbra damage in the executive control area.
6. Dead brain in the executive control area.
7. Penumbra damage in the white matter underlying any of these three.
8. Dead brain in the white matter underlying any of these three.
9. Spasticity preventing movement from occurring.
 CSE research assistant professor Nadir Weibel and CSE Ph.D. student Steven Rick are part of a small, interdisciplinary team that has been awarded a Frontier of Innovation Scholars Program (FISP) grant to pursue a sensor-based approach to multimodal stroke signature.
The so-called Stroke-Kinect team includes colleagues in engineering, computer science and the UC San Diego School of Medicine. Led by CSE’s Weibel — who is also a member of the Design Lab located in the Qualcomm Institute — the project was awarded $50,000, all of which will fund CSE’s Rick and Ph.D. student Vishwajith (Vish) Ramesh in the Department of Bioengineering while they are working over the next year on the technology.
It was one of more than 400 high-caliber proposals submitted as part of this year’s FISP grant solicitation by the university.
CSE’s Steven Rick and Bioengineering’s Vish Ramesh both work in Weibel’s Human-Centered and Ubiquitous Computing Lab. Rick is also a member of the Design Lab’s Human Centered Healthcare team. He did his undergraduate work at UC San Diego in Cognitive Science (B.S. ’13) before switching to CSE. Currently his research focuses on computational ethnography — the augmentation of human observational research with insight from unobtrusive and ubiquitous sensing. In the Design Lab, located on the first floor of Atkinson Hall, Rick helps apply a mix of methodologies toward the generation of better human understanding of health and healthcare coordination. Rick expects to complete his Ph.D. in 2020.
Vish Ramesh
Stroke-Kinect is a new approach to characterizing the severity of ischemic stroke. The system exploits cutting-edge pervasive sensing technologies that unobtrusively capture body motion, eye tracking, and speech. The goal is to use all of these modes of communication and sensing — hence ‚multimodal’ — to understand the dynamics of human behavior and automatically assess clinical deficit scales more frequently and precisely than current human resources allow.
Team members aim to remove the subjectivity of human analysis in characterizing ischemic stroke, and to do so by allowing a more accurate quantification of specific behavioral patterns in individuals who have undergone a stroke. Another benefit of the system will be to enable rapid observation-diagnosis feedback loops by informing clinicians of patient deficits in real time. Weibel and his colleagues — including Bioengineering professor Gert Cauwenberghs and School of Medicine neuroscience professor Brett Meyer (a top expert on stroke) — will leverage campus expertise in neurology, stroke diagnosis and stroke rehabilitation. Stroke-Kinect will also collect and analyze multimodal data in the healthcare domain using pervasive sensing technologies, multi-year experience in neural computation and bioengineering, and via access to Meyer’s UCSD Stroke Clinic.


Who the fuck cares about attitude and perception? Survivors just want to know what results can be achieved.

The Very Best Learning Method Is Not Taught To Students Or Teachers

Would this also apply to relearning movements impacted by your stroke? We'll never know.
The one learning technique which works best is the one that students use the least.
Spreading out learning over time is one of the most effective strategies.
So-called ‘distributed practice’ means breaking up learning into short sessions.
People learn better when they learn in these short sessions spread over a long period of time.
The reverse — cramming in a short space of time — doesn’t work that well.
Despite this, distributed practice is very infrequently used by students and may not be highlighted as a top strategy to them by teachers.
Instead, students tend to use highly inefficient methods such as highlighting, summarising, underlining and re-reading.
One technique that is effective — which students do sometimes use — is testing.
Professor John Dunlosky, one of the study’s authors, said:
“I was shocked that some strategies that students use a lot — such as rereading and highlighting — seem to provide minimal benefits to their learning and performance.
By just replacing rereading with delayed retrieval practice, students would benefit.”
Professor Dunlosky continued:
“These strategies are largely overlooked in the educational psychology textbooks that beginning teachers read, so they don’t get a good introduction to them or how to use them while teaching.”
The frightening thing is that we have known about the power of distributed practice for over a hundred years, and yet people continue to study by cramming.
The study was published in the journal Psychological Science in the Public Interest (Dunlosky et al., 2013).

Scientists develop first Canadian Brain Health Food Guide to help adults preserve thinking, memory skills

Pretty decent, but still just a guide. I would expect exact amounts per body weight to keep the appropriate levels of nutrients for the benefits suggested. This is not rocket science, somebody can do that research. How many decades before your doctor has the hospital nutritionist set up this protocol for hospital food and your at home meals?

Scientists develop first Canadian Brain Health Food Guide to help adults preserve thinking, memory skills

The backfire effect among stroke medical professionals and stroke associations.

   I think that the stroke medical world is going down the completely wrong path(F.A.S.T. and prevention) and the  backfire effect will cause them to dig into their erroneous beliefs. I'm not quite sure that I know how to solve this except to wait for those people to die and then infiltrate the colleges.

Neuroprotective compound could save brain cells during stroke, rat study shows

WHOM do we talk to to get this followed up in humans? Or will this fall thru the cracks like most promising stroke research due to our fucking failures of stroke associations? I bet the lasting effect is because there are less dead and damaged neurons because of the treatment. It stopped some part of the neuronal cascade of death.
Researchers from the University of Iowa Carver College of Medicine and the University of Miami Miller School of Medicine have shown that a neuroprotective compound tested in rats provides two-pronged protection for brain cells during stroke and improves physical and cognitive outcomes in the treated animals.
Every year, nearly 800,000 Americans have a stroke and almost 130,000 die. Survivors often are left with long-term physical and cognitive disability that significantly alters their lives.
When a stroke interrupts the brain's blood supply, mature brain cells (neurons) die. In addition, reestablishing blood flow, known as reperfusion, also leads to processes that cause cell death. A part of the brain's natural response to stroke injury is to increase production of new brain cells in two specific regions (the subgranular zone of the hippocampal dentate gyrus and the subventricular zone of the lateral ventricles), which normally make a smaller number of new brain cells every day. Unfortunately, the vast majority of these newborn cells die within one to two weeks, limiting the benefit of this potential repair process. Minimizing the loss of brain cells is a primary goal for new stroke therapies.
"If we could prevent the mature brain cells from dying that would be beneficial," says Andrew Pieper, MD, PhD, professor of psychiatry in the UI Carver College of Medicine and co-senior study author. "But if we could also support or enhance this surge in neurogenesis (birth of new neurons), we might be able to further foster recovery, especially in terms of cognitive function, which is critically dependent on the hippocampus."
Using rats, Pieper and his colleagues Zachary B. Loris and W. Dalton Dietrich, PhD, tested the effects of a compound called P7C3-A20 on these two aspects of neuroprotection following ischemic stroke. Blood flow to the rats' brains was interrupted for 90 minutes and then the blockage was cleared allowing reperfusion. One group of rats was given the P7C3-A20 compound twice daily for seven days following the stroke. P7C3-A20 has previously been shown to prevent brain cell death in other animal models of neurologic injury, including Parkinson's disease, amyotrophic lateral sclerosis, stress-associated depression, and traumatic brain injury.
In terms of the brain itself, the P7C3-A20 compound reduced loss of brain tissue (atrophy) and increased survival of newborn neurons six weeks after stroke. In addition to the improved survival of both mature and newborn neurons, rats that received the P7C3-A20 compound for seven days after stroke also had better physical and cognitive outcomes than untreated rats. Treated rats had improved balance and coordination one week after stroke, and improved learning and memory one month after stroke. The findings were published recently in the journal Experimental Neurology.
"There is no previous demonstration of a pharmacologic agent that both protects mature neurons from dying and also boosts the net magnitude of neurogenesis," Pieper says. "Our compound is beneficial in this animal model of stroke, and we're hopeful that it might eventually benefit patients."
"Currently there are limited treatments for acute stroke that make a real difference in patient's lives. There is an urgent need to identify, test, and translate new therapies to the clinic," adds Dietrich, co-senior study author and Scientific Director of The Miami Project to Cure Paralysis, professor of neurological surgery, neurology, biomedical engineering and cell biology at the University of Miami where the studies were conducted. "The ability to both protect and repair the injured nervous system has major implications on how we think about improving outcomes in millions of people each year with acute neurological injuries."
The neuronal protection provided by the P7C3-A20 compound was also associated with a boost in the levels of a substance called nicotinamide adenine dinucleotide (NAD) in the rats' brains. NAD is emerging as an important player in neuronal health and survival. Levels of this substance are depleted during stroke, and it has been proposed that increasing NAD levels may be a therapeutic target for treating stroke. In this study, P7C3-A20 treatment restored NAD to normal levels in the rats' cortex after a stroke.
Importantly, the study examined the effects of P7C3-A20 on cognitive and physical outcomes well beyond the time of the initial stroke. The sustained physical and cognitive improvement seen in the rats up to one month after the stroke suggests that the P7C3-A20 compound provides a long-term benefit.
"We found we can give the compound in this critical period immediately after the stroke and it has a lasting effect," notes Pieper, who also is a professor of neurology, radiation oncology, and a psychiatrist with the Iowa City Veterans Affairs Health Care System.
In recent years, advances in treatments that break up or remove stroke-causing blood clots have reduced the death rate for stroke and are improving outcomes for patients. The researchers hope that a treatment based on P7C3-A20 used in addition to the clot-clearing therapies might further improve outcomes by protecting brain cells during the traumatic ischemia/reperfusion period.

Queen’s University researchers make major brain repair discovery in fight against Multiple Sclerosis for myelin repair

First we need to know if myelin is damaged during a stroke. Ask your doctor that question, I have not been able to find a concrete answer.

Queen’s University Belfast scientists have discovered that specific cells from the immune system are key players in brain repair – a fundamental breakthrough that could revolutionise the treatment of debilitating neurological disorders such as Multiple Sclerosis (MS).
The research study, led by Dr Yvonne Dombrowski and Dr Denise Fitzgerald at the Wellcome-Wolfson Institute for Experimental Medicine at Queen’s University Belfast, is being hailed as a landmark study in unravelling the mysteries of how the brain repairs damage. This is crucial in the fight against MS, which affects 2.3 million people world-wide and over 4,500 people in Northern Ireland.
MS is the most common neurological disease affecting young adults and is the result of damage to myelin, the protective sheath surrounding nerve fibres of the central nervous system – the brain, spinal cord and optic nerve. In MS, the immune system wrongly attacks the myelin sheath covering nerve fibres in the brain and spinal cord, which can lead to symptoms such as vision loss, pain, fatigue and paralysis.
Until now, medical treatment could limit relapses but could not reverse the damage already done by the condition. The exciting aspect of this new research is that the team have uncovered beneficial effects of immune cells in myelin repair that have potential to reverse myelin damage. The study was an international collaboration including experts in Cambridge, San Francisco, Edinburgh, Maynooth and Nice.
The research breakthrough, which has been published today in Nature Neuroscience, shows that a protein made by certain cells within the immune system triggers the brain’s stem cells to mature into oligodendrocytes that repair myelin.
The discovery means that researchers can now use this new knowledge to develop medicines which will boost these particular cells and develop an entirely new class of treatments for the future.
Speaking about the importance of the new research, Dr Dombrowski, who is the lead author of the report, explained: “At Queen’s we are taking a unique and fresh approach to uncover how the immune system drives brain repair. This knowledge is essential to designing future treatments that tackle neurological diseases, such as MS, in a new way – repairing damage rather than only reducing attacks. In the future, combining these approaches will deliver better outcomes for patients.”
Senior author of the study, Dr Denise Fitzgerald from Queen’s, experienced a condition similar to MS, called Transverse Myelitis when she was 21 and had to learn to walk again.
Commenting on the findings, Dr Fitzgerald said: “This pioneering research, led by our team at Queen’s, is an exciting collaboration of top scientists from different disciplines at Cambridge, San Francisco, Edinburgh, Maynooth and Nice. It is by bringing together these experts from immunology, neuroscience and stem cell biology that we have been able to make this landmark discovery.
“This is an important step forward in understanding how the brain and spinal cord is naturally repaired and opens up new therapeutic potential for myelin regeneration in patients. We continue to work together to advance knowledge and push the boundaries of scientific knowledge for the benefits of patients and society, in a bid to change lives for the better, across the globe.”
Dr Sorrel Bickley, Head of Biomedical Research at the MS Society, said: “MS is an unpredictable and challenging condition, and we are committed to driving forward research to find effective treatments for everyone. This exciting study gives us an important understanding of how myelin repair can be promoted, which could open up new areas for treatment development. We welcome this international collaboration led by Northern Ireland, where rates of MS are amongst the highest in the world.”
This work was supported by a number of funders including the BBSRC, Wellcome Trust, Leverhulme Trust and the UK MS Society.

Attached files

  • Many mature oligos_red-myelin_green-oligodendrocyte cell

  • Dr Yvonne Dombrowski

  • Dr Denise Fitzgerald

Buzzing the brain with electricity can boost working memory

Conflicting reports on this, so ask your doctor for proof one way or another.

Bad news for DARPA's RAM program: Electrical Stimulation of Entorhinal Region Impairs Memory

Buzzing the brain with electricity can boost working memory

Scientists have uncovered a method for improving short-term working memory, by stimulating the brain with electricity to synchronise brain waves.
Researchers at Imperial College London found that applying a low voltage current can bring different areas of the brain in sync with one another, enabling people to perform better on tasks involving working memory.
The hope is that the approach could one day be used to bypass damaged areas of the brain and relay signals in people with traumatic brain injury, stroke or epilepsy.
The brain is in constant state of chatter, with this activity seen as brainwaves oscillating at different frequencies and different regions keeping a steady ‘beat’.
In a small study, published today in the journal eLife, the Imperial team found that applying a weak electrical current through the scalp helped to align different parts of the brain, synchronising their brain waves and enabling them to keep the same beat.
“What we observed is that people performed better when the two waves had the same rhythm and at the same time,” said Dr Ines Ribeiro Violante, a neuroscientist in the Department of Medicine at Imperial, who led the research.
In the trial, carried out in collaboration with University College London, the team used a technique called transcranial alternating current stimulation (TACS) to manipulate the brain’s regular rhythm.
They found that buzzing the brain with electricity could give a performance boost to the same memory processes used when people try to remember names at a party, telephone numbers, or even a short grocery list.
Dr Violante and team used TCAS to target two brain regions – the middle frontal gyrus and the inferior parietal lobule – which are known to be involved in working memory.
Ten volunteers were asked to carry out a set of memory tasks of increasing difficulty while receiving theta frequency stimulation to the two brain regions at slightly different times (unsynchronised), at the same time (synchronous), or only a quick burst (sham) to give the impression of receiving full treatment.
In the working memory experiments, participants looked at a screen on which numbers flashed up and had to remember if a number was the same as the previous, or in the case of the harder trial, if it the current number matched that of two-numbers previous.
Results showed that when the brain regions were stimulated in sync, reaction times on the memory tasks improved, especially on the harder of the tasks requiring volunteers to hold two strings of numbers in their minds.
“The classic behaviour is to do slower on the harder cognitive task, but people performed faster with synchronised stimulation and as fast as on the simpler task,” said Dr Violante.
Previous studies have shown that brain stimulation with electromagnetic waves or electrical current can have an effect on brain activity, the field has remained controversial due to a lack of reproducibility.
But using functional MRI to image the brain enabled the team to show changes in activity occurring during stimulation, with the electrical current potentially modulating the flow of information.
“We can use TACS to manipulate the activity of key brain networks and we can see what’s happening with fMRI,” explained Dr Violante.
“The results show that when the stimulation was in sync, there was an increase in activity in those regions involved in the task. When it was out of sync the opposite effect was seen.”
However, one of the major hurdles for making such a treatment widely available is the individual nature of people’s brains. Not only do the electrodes have to get the right frequency, but target it to the right part of the brain and get the beat in time.
Dr Violante added: “We use a very cheap technique, and that's one of the advantages we hope it will bring if it's translatable to the clinic.
“The next step is to see if the brain stimulation works in patients with brain injury, in combination with brain imaging, where patients have lesions which impair long range communication in their brains.
“The hope is that it could eventually be used for these patients, or even those who have suffered a stroke or who have epilepsy.”
Professor David Sharp, a neurologist in Imperial’s Department of Medicine and senior author on the paper, added: “We are very excited about the potential of brain stimulation to treat patients. I work with patients who often have major problems with working memory after their head injuries, so it would be great to have a way to enhance our current treatments, which may not always work for them.
“Our next step is to try the approach out in our patients and we will see whether combining it with cognitive training can restore lost skills.”

Attached files

  • Brain activation patterns during stimulation. The scans showed that stimulation ‘in beat’ increases brain activity in the regions involved in task performance. On the other hand, stimulation ‘out of beat’ showed activity in regions usually associated with resting. (credit: Ines Violante)

Tuesday, March 14, 2017

Herpes Zoster and the Risk of Stroke in Patients with Autoimmune Diseases - CME

Not how to get survivors 100% recovered but another risk for stroke, probably with nothing even suggested to ameliorate that risk.

Credit: 0.50 CME
Cleveland Clinic Center for Continuing Education

“Tele-health, wearable sensors and the Internet. Will they improve stroke outcomes through increased intensity of therapy, motivation and adherence to rehabilitation programs?”

Once again laying the complete stroke recovery upon the survivors. Your doctor and therapists essentially do nothing but act as nagging coaches.
The following article has just been accepted for publication in Journal of Neurologic Physical Therapy:
“Tele-health, wearable sensors and the Internet. Will they improve stroke outcomes through increased intensity of therapy, motivation and adherence to rehabilitation programs?”
Jane Helena Burridge, PhD; Ruth Turk, PhD; Maria Stokes, PhD; Jill Whitall, PhD; Ravi Vaidyanathan, PhD; Phil Clatworthy, PhD; Lucy Yardley, PhD; Ann-Marie Hughes, PhD; Claire Meagher, MSc; Alan Chong W Lee, PhD, DPT, CWS, GCS; Enrico Franco, PhD
Provisional Abstract:
Background and Purpose
Stroke, predominantly a condition of older age, is a major cause of acquired disability in the global population and puts an increasing burden on healthcare resources. Clear evidence for the importance of intensity of therapy in optimizing functional outcomes is founded in animal models, supported by neuroimaging and behavioral research, and strengthened by recent meta-analyses from multiple clinical trials. However, providing intensive therapy using conventional treatment paradigms is expensive and sometimes not feasible due to patients’ environmental factors. This paper addresses the need for cost-effective increased intensity of practice and suggests potential benefits of telehealth (TH) as an innovative model of care in physical therapy.
Summary of Key Points
We provide an overview of TH and present evidence that a web-supported program used in conjunction with Constraint Induced Therapy (CIT), can increase intensity and adherence to a rehabilitation regimen. The design and feasibility testing of this web-based program, ‘LifeCIT’ is presented. We describe how wearable sensors can monitor activity and provide feedback to patients and therapists. The methodology for the development of a wearable device with embedded inertial measurement units and mechanomyography sensors, algorithms to classify functional movement, and a graphical user interface to present meaningful data to patients to support a home exercise program is explained.
Recommendations for Clinical Practice
We propose that wearable sensor technologies and TH programs have the potential to provide cost-effective, intensive, home-based stroke rehabilitation.
Want to read the published article?
To be alerted when this article is published, please sign up for the Journal of Neurologic Physical Therapy eTOC.

Weekend in Pittsburgh

Saw the Andy Warhol museum, went to lunch with Amy and Pat. Fun times. Didn't realize his involvement in music and film. Last year saw his Glenn Close extreme closeup in the Toledo Art Museum.
A Map of the Open Country of a Woman's Heart
High School graduation 1945

Choosing the Right Stroke Rehab Facility

Totally worthless information. What is needed is factual information on 30-day deaths, 100% recovery, efficacy of all stroke protocols. None of which I have ever seen reported by any  rehabilitation provider.
Knowing where to turn for rehabilitation and support after a stroke can be overwhelming, according to expert volunteers from the American Stroke Association, which published its first-ever Guidelines for Stroke Rehabilitation and Recovery for Adults.
Stroke rehabilitation often requires healthcare professionals from several disciplines because a stroke can affect many functions: paralysis and weakness; gross and fine motor skills; speech and language; cognition; vision; and emotions. Yet limited timeframes to find care after discharge can be challenging.
Knowing where to turn for rehabilitation and support after a stroke can be overwhelming, according to expert volunteers from the American Stroke Association, which published its first-ever Guidelines for Stroke Rehabilitation and Recovery for Adults.

“There is increasing evidence that rehabilitation can have a big impact on survivors’ quality of life, so the time is right to review the evidence in this complex field and highlight effective and important aspects of rehabilitation,” said Carolee J. Winstein, Ph.D., lead author of the scientific statement published in the May 2016 issue of the American Heart Association journal Stroke.
Stroke rehabilitation often requires healthcare professionals from several disciplines because a stroke can affect many functions: paralysis and weakness; gross and fine motor skills; speech and language; cognition; vision; and emotions. Yet limited timeframes to find care after discharge can be challenging. The average hospital stay in acute care is between four (ischemic) and seven days (hemorrhagic stroke). Most stroke patients are transferred from acute care to an inpatient rehabilitation facility (IRF); a skilled nursing facility (SNF) or a long-term acute care (LTAC) hospital. Those discharged to home may have home health, outpatient therapy, or hospice care.
Rehab dollars should be used wisely, and at an inpatient rehabilitation facility if possible, Winstein said. Families should first check with their insurance plan to see what types of post-acute care are covered. Evaluating inpatient rehabilitation facilities and skilled nursing facilities? Here’s a short breakdown of the services both provide, and questions to ask:
Inpatient rehab facilities typically take a team approach, with therapists meeting to discuss patient care. The patient must be able to participate in three hours of therapy every day. Medicare will cover up to 90 days in an inpatient rehab facility (or longer in some instances, although cost sharing is very high). is launching a public quality rating program for IRFs this fall.
If a patient can’t participate in three hours of daily therapy, a skilled nursing facility with a coordinated rehab program may be able to provide care, but resources, facility and programs provided vary, and finding the right place may require some investigation. Medicare will usually cover up to 100 days. posts public quality ratings for skilled nursing facilities, a good way to evaluate facilities apples-to-apples with specific quality measures.
(Also see “Commission on Accreditation of Rehabilitation Facilities.”)
Patients discharged from the hospital directly home may receive rehabilitation services from a home health agency or on an outpatient basis. Medicare covers up to 60 days of home health services. Insurance limits on outpatient therapy services can be as short as 2-3 weeks for physical, occupational and speech therapy, but Medicare has an “exceptions process” that allows patients to receive additional outpatient therapy if medically necessary.

Safety and Efficacy of Remote Ischemic Preconditioning in Patients with Severe Carotid Artery Stenosis Prior to Carotid Artery Stenting: A Proof-of-Concept, Randomized Controlled Trial

I wonder why closing up of the carotid artery is not considered if the Circle of Willis is complete rather than go thru the risks of stenting or endarterectomy.
Zhao W, Meng R, Ma C, Hou B, Jiao L, Zhu F, Wu W, Shi J, Duan Y, Zhang R, Zhang J, Sun Y, Zhang H, Ling F, Wang Y, Feng W, Ding Y, Ovbiagele B, Ji X; Circulation (Feb 2017)
BACKGROUND -Remote ischemic preconditioning (RIPC) can inhibit recurrent ischemic events effectively in patients with acute or chronic cerebral ischemia. However, it is still unclear that whether RIPC can impede ischemic injury after carotid artery stenting (CAS) in patients with severe carotid artery stenosis.
METHODS -Subjects with severe carotid artery stenosis were recruited in this randomized controlled study, and assigned to RIPC, sham and no intervention (control) groups. All subjects received standard medical therapy. Subjects in the RIPC and sham groups underwent RIPC and sham RIPC twice daily respectively for 2 weeks prior to CAS. Plasma NSE and S-100B were used to evaluate safety, hypersensitive C-reactive protein (hs-CRP) and new ischemic DWI lesions were used to determine treatment efficacy. The primary outcomes were the presence of ≥ 1 newly ischemic brain lesions on DWI within 48 hours after stenting and clinical events within 6 months after stenting.
RESULTS -We randomized 189 subjects in this study (63 subjects in each group). Both RIPC and sham RIPC procedures were well tolerated and completed with high compliance (98.41% and 95.24% respectively). Neither plasma NSE levels nor S-100B levels changed significantly before and after treatment. No severe adverse event was attributed to RIPC and sham RIPC procedures. The incidence of new DWI lesions in the RIPC group (15.87%) was significantly lower than the sham group (36.51%; RR 0.44; 96% CI 0.20 to 0.91, p<0.01) and the control group (41.27%; RR 0.39, 96% CI 0.21 to 0.82; p<0.01). The volumes of lesions were smaller in the RIPC group compared to the control and sham groups (p<0.01 each). Ischemic events occurred after CAS were 1 TIA in RIPC group, 2 strokes in control group and two strokes and one TIA in sham group, but these results were not significantly different among three groups (p=0.597).
CONCLUSIONS -RIPC is safe in patients undergoing CAS, which may be able to decrease ischemic brain injury secondary to CAS. However, the mechanisms and effects of RIPC on clinical outcomes in this cohort of patients need further investigation.Clinical Trial Registration-URL: Unique identifier: NCT01654666.

Buyang Huanwu Decoction Ameliorates Poststroke Depression via Promoting Neurotrophic Pathway Mediated Neuroprotection and Neurogenesis

You can read this on your own but since it is in the Evidence-based Complementary and Alternative Medicine Journal it is already is suspect in the proofs provided. Only 10 pages.

Buyang Huanwu Decoction Ameliorates Poststroke Depression via Promoting Neurotrophic Pathway Mediated Neuroprotection and Neurogenesis

Effects of different exercise strategies and intensities on memory performance and neurogenesis

Maybe there is a protocol in the full article but I doubt it, making this totally useless.
Kai Diederich1*, Anna Bastl1, Heike Wersching2, Anja Teuber2, Jan-Kolja Strecker1, Antje Schmidt1, Jens Minnerup1 and Wolf-Rüdiger Schäbitz3
  • 1Department of Neurology, University of Münster, Germany
  • 2Institute of Epidemiology and Social Medicine, University of Münster, Germany
  • 3Department of Neurology, Evangelisches Krankenhaus Bielefeld, Germany
It is well established that physical exercise affects both hippocampal neurogenesis and memory functions. Until now, distinctive effects of controlled and voluntary training on behavior and neurogenesis as well as interactions between exercise intensity, neurogenesis and memory performance are still elusive. The present study tested the impact of moderate controlled and voluntary training on memory formation and hippocampal neurogenesis and evaluated interactions between exercise performance, learning efficiency and proliferation of progenitor cells in the hippocampus.
Our data show that both controlled and voluntary training augmented spatial learning and promoted hippocampal neurogenesis. Regression analysis revealed a significant linear increase of the amount of new hippocampal neurons with increased exercise intensity. Regression analysis of exercise performance on retention memory performance revealed a quadratic, inverted u-shaped relationship between exercise performance and retention of spatial memory. No association was found between the amount of newborn neurons and memory performance.
Our results demonstrate that controlled training, if performed with an appropriate combination of speed and duration, improves memory performance and neurogenesis. Voluntary exercise elevates neurogenesis dose dependently to high levels. Best cognitive improvement was achieved with moderate exercise performance.
Keywords: Exercise, Hippocampal neurogenesis, Learning, Memory, Regression Analysis
Citation: Diederich K, Bastl A, Wersching H, Teuber A, Strecker J, Schmidt A, Minnerup J and Schäbitz W (2017). Effects of different exercise strategies and intensities on memory performance and neurogenesis. Front. Behav. Neurosci. 11:47. doi: 10.3389/fnbeh.2017.00047

Visual effects and rehabilitation after stroke

You will notice that none of the treatment options have the doctor doing one damn thing. Adaptation, not cure. You are on your own.
trokes, or cerebrovascular accidents (CVA) are common, particularly in older people. The problems of motor function and speech are well known. This article explains the common visual problems which can occur with a stroke and gives information about diagnosis and management.

What is a stroke?

A stroke occurs when there is an interruption to blood flow to the brain either because of a blood clot blocking the blood vessel or a haemorrhage in the brain.1 Strokes can cause signs which are obvious, such as loss of speech, drooping of one side of their face, or weakness or paralysis of the arm and/or leg on one side of the body.1 The vision is affected in about two thirds of people who have had a stroke, but this is often not obvious to the patient or their carers. For example, someone who has weakness down one side may bump into things or not eat all the food on their plate, not realising that this may also be because they have visual field loss.2

What causes a stroke?

A stroke or cerebrovascular accident, (CVA) is the result of a blocked blood vessel in the brain (thrombosis or embolus), or haemorrhage into the brain.1 Strokes are more likely in the elderly, and those who have high blood pressure, diabetes or cardiovascular disease.

Types of visual loss in people who have had a stroke

There are four ways in which vision can be affected following a stroke:
  1. Loss of central vision
  2. Visual field loss
  3. Visual perceptual abnormalities
  4. Eye movement abnormalities
These may occur in isolation but more frequently occur in combination.3 Problems with central vision are quite common after a stroke. The symptoms include blurred or altered vision. In many the vision improves, but the visual loss can be permanent.
Visual field loss occurs in up to half of people with a stroke, with the commonest defect being homonymous hemianopia in which vision is lost in the right or the left visual fields (Figure 1).4 Patients may not be aware of this, and bump into door frames or trip over things on the affected side. Reading can also be difficult (Figure 2).

Image showing loss of field of vision in both eyes
Figure 1. Right homonymous hemianopia: the right-hand field of view is lost in both eyes
Image illustrating how a page of text appears to someone with double vision and someone with right hemianopia
Figure 2. Impact of vertical double vision (central image) and right hemianopia (right image) on reading
Visual perceptual deficits are many and varied affecting about a third of people with a stroke. Problems that may develop include neglect one side of their body; difficulty recognising faces or objects, or difficulties with colour vision, depth perception and motion.5 Eye movement abnormalities can also be varied, including strabismus (misaligned eyes), difficulty in converging the eyes to look at near objects, or double vision due to the cranial nerves which control eye movement being affected.6 Typical symptoms include double vision, or jumbled, blurred and/or juddery vision (Figure 2).


Blurred vision, double vision and lossand loss of visual field are significant symptoms that impair daily functioning.7 The patient or their close relatives may report that they frequently bump into objects such as door frames; have difficulty finding things on surfaces; are unsure of their footing while walking and stumble; may leave food uneaten on one side of the plate and have difficulty with reading. Other impacts on the quality of life include loss of confidence, fear of falling, fear of going out alone, social isolation and loss of independence.8

How to assess visual function in someone who has had a stroke

Examination for visual loss is essential for stroke survivors.9 There are various assessment tools which can be used to examine visual function after a stroke:


Treatment options aim to restore visual function to as normal as possible.10 For eye movement abnormalities,prisms and patching one eye can be effective in reducing double vision.6 For visual field loss a Cochrane systematic review reports favourable evidence of visual scanning training which aims to compensate for the visual field loss.11 It is available as a paper training option ( or through computer training (;
Stroke survivors with persistent impairment of central vision may be helped by low vision services which can include magnifiers, reading aids, computerised adaptations and improved lighting.12 Furthermore, simple adaptations can be made by stroke survivors such as using large print, ensuring good lighting at home, putting labels or coloured stickers on cooking equipment, decluttering areas and having a companion when going out, particularly in busy, crowded places.10


Post-stroke difficulties in visual function are an under-recognised problem that cause significant impact to the quality of life of stroke survivors. Carers and health workers need to be aware that problems with vision are a common consequence of stroke that is not outwardly obvious. Assessment including visual functioning is best provided as part of a multi-disciplinary team on acute stroke units, or in neuro-rehabilitation units. A careful history about visual problems from the patient and carers followed by examination of visual acuity, eye movements and visual field are important in understanding the difficulties in visual functioning.
Management should be tailored to each individual, their visual difficulties and visual needs. With about one quarter of stroke survivors being of working age, rehabilitation in the conext of adaptation of the work place environment is vital if younger people are to return to work after stroke. Rehabilitation requires patience and perseverance on the side of the client, relatives and the health provider.
Despite improvement in stroke prevention and acute stroke management, the increasing ageing population will result in more stroke survivors requiring rehabilitation. Policy makers need to understand the importance of providing post-stroke rehabilitation services including visual functioning.