Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Friday, May 31, 2019

Happy ever after: 25 ways to live well into old age

I won't do the work longer part, that to me is stupid.  I was burning up my health by working, it may have been good cognitively but I was coasting, nothing was that challenging.

Happy ever after: 25 ways to live well into old age

Stroke study finds mouth bacteria in brain clots Stroke Study Finds Mouth Bacteria In Brain Clots

Is your doctor taking responsibility to make sure you know EXACTLY what needs to be done to keep this oral bacteria at bay? Did you get recovered enough to brush your teeth with your affected hand? That is the definition of recovery you should expect.

Stroke Study Finds Mouth Bacteria In Brain Clots

(@imziishan)
Stroke study finds mouth bacteria in brain clots

Researchers from Tampere University in Finland analyzed clot samples from 75 people who received emergency treatment for ischemic stroke when they attended Tampere University Hospital's Acute Stroke Unit

ISLAMABAD (UrduPoint / Pakistan Point News / Online - 31st May, 2019) Researchers from Tampere University in Finland analyzed clot samples from 75 people who received emergency treatment for ischemic stroke when they attended Tampere University Hospital's Acute Stroke Unit.The patients had undergone thrombectomies.
These procedures remove blood clots by means of catheters conducted through arteries. The catheters can deploy stent retrievers and aspirators to reduce or remove the clot.When they analyzed blood clots sampled in this way, the researchers found that 79% of them bore DNA from common oral bacteria.
Most of the bacteria were of the Streptococcus mitis type, which belong to a group that scientists call viridans streptococci.The levels of the oral bacteria were much higher in the blood clot samples than they were in other samples that surgeons took from the same patients.
The team reports the findings in a recent Journal of the American Heart Association study.The study forms part of a large investigation that Tampere University has been conducting for around 10 years on the role of bacteria in cardiovascular diseases.This investigation has already found that blood clots that have caused heart attacks, brain aneurysms, and thromboses in leg veins and arteries, contain oral bacteria, particularly viridans streptococci.
It has also shown that these bacteria can cause infective endocarditic, a type of heart infection.The researchers believe that the new study is the first to implicate viridans streptococci in acute ischemic stroke.A stroke is when the brain suddenly experiences a disruption to its blood supply.
This starves cells of essential oxygen and nutrients and can result in tissue damage and loss of function in the brain.The most common type of stroke is an ischemic stroke, which occurs when a blood clot reduces the blood supply in an artery that feeds the brain.According to figures from the World Stroke Organization, around 1 in 6 people worldwide will likely experience a stroke in their lifetime.One of the leading causes of stroke is a condition called atherosclerosis in which plaques form in the walls of arteries and cause them to narrow and harden over time.
The plaques are deposits of cellular waste, fat, cholesterol, and other materials.Depending on where the plaques form, atherosclerosis can raise the risk of heart disease, angina, carotid artery disease, and peripheral artery disease.However, plaques can also lose bits into the bloodstream, or attract clots.
If such an event affects an artery supplying blood to the brain, it can trigger an ischemic stroke

Alteplase effective up to 9 hours after ischemic stroke

Then your definition of effective is an appallingly low bar. 100% recovery is my definition. WHEN THE HELL WILL YOU EVEN TRY TO GET THERE?

You might want to talk to stroke survivors sometime and compare what they want vs. what you are attempting to do. 

Alteplase effective up to 9 hours after ischemic stroke

Bruce C.V. Campbell
Bruce C.V. Campbell
In a meta-analysis presented at the European Stroke Organization Conference, alteplase was more effective than placebo for treatment of acute ischemic stroke between 4.5 and 9 hours after onset.
Guidelines recommend the use of a tissue plasminogen activator such as alteplase within 4.5 hours of acute ischemic stroke onset, but the researchers analyzed whether perfusion imaging could identify whether patients could benefit from alteplase after 4.5 hours or upon waking up with stroke symptoms.
Bruce C.V. Campbell, PhD, professor of medicine at Melbourne Brain Centre and Royal Melbourne Hospital, University of Melbourne, Australia, and colleagues conducted a systematic review and meta-analysis of 414 patients from three trials who were assigned alteplase (mean age, 73 years; 56% men) or placebo (mean age, 72 years; 58% men) after waking up with acute ischemic stroke symptoms or presenting with them between 4.5 and 9 hours after onset and were imaged with CT perfusion or perfusion-diffusion MRI. The results were simultaneously published in The Lancet.
The primary outcome was excellent functional outcome, defined as a modified Rankin Scale (mRS) score of 0 or 1, at 3 months.
The primary outcome was achieved in 36% of patients in the alteplase group and 29% of the placebo group (adjusted OR = 1.86; 95% CI, 1.15-2.99), according to the researchers.
Symptomatic intracranial hemorrhage occurred in 5% of the alteplase group vs. less than 1% of the placebo group (aOR = 9.7; 95% CI, 1.23-76.55).
“However, this did not negate the benefit of alteplase in ordinal analysis of the mRS, which accounts for transitions across the disability spectrum,” Campbell and colleagues wrote in The Lancet.
There was no significant difference between the groups in mortality (alteplase, 14%; placebo, 9%; aOR = 1.55; 95% CI, 0.81-2.96).
“This pooled analysis provides strong evidence in support of thrombolysis for patients with favorable perfusion imaging 4.5 to 9 hours after stroke, including patients with wake-up stroke,” Campbell and colleagues wrote.
In a related editorial in The Lancet, Shelagh B. Coutts, MD, MSc, and Bijoy K. Menon, MBBS, MD, MSc, both associate professors of medicine at the University of Calgary, wrote, “These findings should not prevent referral of a patient for endovascular clot retrieval, but might allow the use of thrombolysis as a bridge therapy during transport or a stand-alone treatment in settings where endovascular clot retrieval is not available.” – by Erik Swain

In a meta-analysis presented at the European Stroke Organization Conference, alteplase was more effective than placebo for treatment of acute ischemic stroke between 4.5 and 9 hours after onset.
Source: Adobe Stock
References:
Campbell BCV, et al. Official Welcome and Large Clinical Trials. Presented at: European Stroke Organization; May 22-24, 2019; Milan.
Campbell BCV, et al. Lancet. 2019;doi:10.1016/S0140-6736(19)31053-0.
Coutts SB, et al. Lancet. 2019;doi:10.1016/S0140-6736(19)31095-5.
Disclosures: Campbell reports no relevant financial disclosures. Please see the study for all other authors’ relevant financial disclosures.

Association of retirement age with mortality: a population-based longitudinal study among older adults in the USA

You will want your doctor to analyze why these came up with totally opposite conclusions. Traveling for work was pounding my body and mind, second best thing I ever did was early retirement at 62, first was having the stroke.

Retire at 55 and live to 80; work till you’re 65 and die at 67. Startling new data shows how work pounds older bodies

The latest here:

Association of retirement age with mortality: a population-based longitudinal study among older adults in the USA 

  1. Chenkai Wu1,
  2. Michelle C Odden1,
  3. Gwenith G Fisher2,
  4. Robert S Stawski3

Abstract

Background Retirement is an important transitional process in later life. Despite a large body of research examining the impacts of health on retirement, questions still remain regarding the association of retirement age with survival. We aimed to examine the association between retirement age and mortality among healthy and unhealthy retirees and to investigate whether sociodemographic factors modified this association.
Methods On the basis of the Health and Retirement Study, 2956 participants who were working at baseline (1992) and completely retired during the follow-up period from 1992 to 2010 were included. Healthy retirees (n=1934) were defined as individuals who self-reported health was not an important reason to retire. The association of retirement age with all-cause mortality was analysed using the Cox model. Sociodemographic effect modifiers of the relation were examined.
Results Over the study period, 234 healthy and 262 unhealthy retirees died. Among healthy retirees, a 1-year older age at retirement was associated with an 11% lower risk of all-cause mortality (95% CI 8% to 15%), independent of a wide range of sociodemographic, lifestyle and health confounders. Similarly, unhealthy retirees (n=1022) had a lower all-cause mortality risk when retiring later (HR 0.91, 95% CI 0.88 to 0.94). None of the sociodemographic factors were found to modify the association of retirement age with all-cause mortality.
Conclusions Early retirement may be a risk factor for mortality and prolonged working life may provide survival benefits among US adults.

10,000 Steps A Day? How Many You Really Need To Boost Longevity - 4,400

It is your doctor's responsibility to get you recovered enough by the time you leave the hospital to do those steps.  Don't let them shirk that responsibility.  So I can get done in 1 hour instead of two hours.

10,000 Steps A Day? How Many You Really Need To Boost Longevity - 4,400




New research shows that daily light walking is important for maintaining health as you age. But if you can't hit 10,000 steps, don't worry.
Peter Muller/Getty Images/Cultura RF
There's nothing magical about the number 10,000.
In fact, the idea of walking at least 10,000 steps a day for health goes back decades to a marketing campaign launched in Japan to promote a pedometer. And, in subsequent years, it was adopted in the U.S. as a goal to promote good health. It's often the default setting on fitness trackers, but what's it really based on?
"The original basis of the number was not scientifically determined," says researcher I-Min Lee of Brigham and Women's Hospital.
She was curious to know how many steps you need to take a day to maintain good health and live a long life, so she and her colleagues designed a study that included about 17,000 older women. Their average age was 72. The women all agreed to clip on wearable devices to track their steps as they went about their day-to-day activities.
It turns out that women who took about 4,000 steps per day got a boost in longevity, compared with women who took fewer steps. "It was sort of surprising," Lee says.
Article continues after sponsor message

In fact, women who took 4,400 steps per day, on average, were about 40 percent less likely to die during the follow-up period of about four years compared with women who took 2,700 steps. The findings were published Wednesday in JAMA Internal Medicine.
Another surprise: The benefits of walking maxed out at about 7,500 steps. In other words, women who walked more than 7,500 steps per day saw no additional boost in longevity.
"I love this study. I think it's really good news for women who may not be particularly active," says Kathleen Janz, who studies how physical activity influences health at the University of Iowa. She was not involved in this study.
Janz, who helped shape the new federal exercise recommendations released last November, says the message that comes from this study is that older women can benefit from just light walking.

"They didn't need to go the gym or invest in a personal trainer or exercise equipment," she says. All they had to do was walk.
And Janz says that's encouraging.
"To me, this study suggests there's more benefit to light activity than we were previously thinking there might be," she says.
Of course, the researchers point out, they would like to know much more about how walking may affect other health parameters such as quality of life and memory and cognitive function. It's possible that walking a greater number of steps each day could influence these outcomes.
Another thing Janz notes is that this study only measures walking. It didn't measure things that many of us do that don't require steps, things like gardening, swimming or biking. And it's safe to assume some women in the study were doing these other things that can influence health as well.
And Janz says to remember the federal exercise guidelines call for 150 minutes per week of moderate physical activity, which includes all kinds of daily movement, not just steps.
So, if 10,000 steps has been feeling out of reach to you, it may be time reset those factory settings on your fitness tracker. Instead, try to hit at least 4,400 a day, along with daily activities that you enjoy. And stick to it.

Why we should say no to positivity — and yes to our negative emotions

I'm hearing it is ok to scream at your doctor for not providing ANY ROUTE TO RECOVERY. I disagree with the be polite statement.  

Why we should say no to positivity — and yes to our negative emotions

May 8, 2019 / +

It sounds paradoxical, but accepting our negative emotions can actually make us happier in the long run. Psychologist Susan David explains how.This post is part of TED’s “How to Be a Better Human” series, each of which contains a piece of helpful advice from someone in the TED community; browse through all the posts here.

Most of us have been told to “Cheer up” or “Look on the bright side” by well-meaning family and friends. Sometimes, it’s because they see us looking sad, angry, anxious or frustrated, but it can also happen because we look pensive, uncertain or just about any state other than joyful. While we may be tempted to tell them “Stuff it,” we don’t because, well, feelings.
Next time, feel free to do so (but please be polite). “Being positive has become a new form of moral correctness,” says psychologist Susan David, founder and codirector of the Institute of Coaching at McLean Hospital of Harvard University Medical School, an instructor in psychology at Harvard, and author of Emotional Agility (read an excerpt here).
Suppressing or turning away from our difficult emotions is not healthy or helpful, says David. “What happens is, it undermines our ability to deal with the world as it is, not as we wish it to be,” she says. “This is associated with lower levels of resilience, lower levels of wellbeing, and higher levels of depression and anxiety. And it also impacts our relationships and our ability to achieve our goals.”
So, what should we do instead?
“Instead of pushing it aside or forcing positivity, one critical way of dealing with a difficult emotion is to label it effectively. In my work, so often people will use very black-and-white labels to describe how they’re feeling,” says David. “‘Stressed’ is one of the most common ones. But there’s a world of difference between the stress of true overwhelm, stress because you’re disappointed, or the stress of knowing you’re in the wrong job or the wrong relationship. When we can label our emotions more accurately, it helps us understand the cause of those emotions and activates what’s called a ‘readiness potential,’ your ability to set goals and to make real concrete changes.”
Next, when you identify your emotion, “notice the emotion with compassion. People frequently think that compassion is about being weak or lazy or lying to yourself,” says David. “Actually compassion allows you to create a safe space within yourself in which you are then able to take more risks. You’re able to explore the world, and you’re able to be more effective, because you know that if things don’t go right that you will still like yourself, you’ll still be kind to yourself. Compassion is associated with greater levels of effectiveness.”
Finally, “try to notice the emotional story for what it is,” says David. Create some space between you and what you’re feeling by acting as an observer and naming all the dimensions of your experience. Instead of simply saying “I’m sad,” she suggests, “say something like, ‘I’m noticing that I’m feeling sad, I’m noticing that I’m feeling undermined, I’m noticing the urge to leave the room.’ This allows you to bring other parts of yourself — such as your values and your intentions — forward.” Doing this also puts you in charge rather than the emotion. “What’s more important is not whether you have negative thoughts or emotions but whether you get hooked into them,” she says, “which is when those thoughts start to drive your behaviors and your interactions.”
Watch her TEDWomen Talk now:

Could Repeated Squeezes to the Arms, Legs Protect the Brain?

Useless for us, young healthy people were used in the experiment. And I never expect any followup from our stroke leaders or researchers.

Could Repeated Squeezes to the Arms, Legs Protect the Brain?


MINNEAPOLIS – What if wearing a blood pressure cuff could help prevent stroke? In a new study, people who restricted their blood flow by wearing inflated blood pressure cuffs on an arm and leg showed signs of more controlled blood flow to their brain, a process that could be protective if blood flow is more severely restricted in the event of a stroke, according at a study published in the May 29, 2019, online issue of Neurology®, the medical journal of the American Academy of Neurology. The process is called remote ischemic preconditioning. Previous studies have shown that remote ischemic preconditioning, using compression on the extremities to repeatedly restrict blood flow and the oxygen it carries, is beneficial to internal organs like the heart, making them more resilient and resistant to changes in blood flow and the serious damage that can occur during a heart attack when tissue is first deprived of oxygen and then damaged when oxygen is restored. “Since previous studies have shown benefits to the heart, we wanted to determine if remote ischemic preconditioning could also be beneficial to the brain,” said study author Yi Yang, MD, PhD, of the First Hospital of Jilin University in Changchun, China. “Our study found such preconditioning temporarily improved dynamic cerebral autoregulation, which is the brain’s ability to regulate and ensure adequate blood flow to the brain despite blood pressure changes. We also found an increase in biomarkers in the blood that can be protective to the nervous system and brain.” The study involved 50 people with an average age of 35 who were all in good health. Each person was monitored twice, for 24 hours each time, first without preconditioning and then with preconditioning. Each participant went through the preconditioning process once, with blood pressure cuffs placed on one upper arm and one thigh. The cuffs were inflated for five minutes and then deflated for five minutes. This process to reduce blood flow was repeated four times. Researchers measured each participant’s brain blood flow regulation by measuring blood pressure and also using ultrasound to measure blood flow within two main arteries in the brain. Measurements were taken at the start of each day and then at six additional time points throughout each 24-hour time period. They found that after preconditioning, participants had improved brain blood flow regulation starting six hours after preconditioning that was sustained for at least 24 hours. Researchers also measured biomarkers in the blood one hour after preconditioning and found that after preconditioning, participants had an increase in two biomarkers known to protect the nervous system, as well as an increase in four biomarkers involved in the inflammatory process in the immune system. They also found lower levels of a biomarker that responds to inflammation. “Our results showed an increase in one biomarker called glial cell line-derived neurotrophic factor that has been previously shown to provide protection not only against diseases such as stroke, but also against other nerve-related diseases like Parkinson’s disease and epilepsy,” said Yang. “Therefore, our results suggest that remote ischemic preconditioning may increase such protective biomarkers and may be beneficial in preventing a number of neurological diseases.” Glial cell line-derived neurotrophic factor increased from an average of 0.289 picograms per milliliter (pg/ml) to an average of 0.789 pg/ml one hour after preconditioning. Yang said, “While our results are exciting, obviously we can’t know when someone will have a stroke and when this could be beneficial. We hope to use these results to help develop a new medication or treatment that will help all people better resist stroke or other neurological diseases. It’s important to emphasize that people should not try to restrict blood flow on their own because, unless under the care of a physician, they could cause themselves harm. In addition, our study was small and much more research needs to be done to confirm our findings before recommendations can be made to physicians to use such preconditioning as a therapy.” One limitation of the study is that blood samples were taken only once. Another limitation is that participants were healthy, so the results may be different in people who have risk factors for stroke or other diseases. The study was supported by the National Key Research and Development Program of China and the Jilin University Science and Technology Innovative Research Team. Learn more about the brain at BrainandLife.org, home of the American Academy of Neurology’s free patient and caregiver magazine focused on the intersection of neurologic disease and brain health. Follow Brain & Life® on Facebook, Twitter and Instagram.
The American Academy of Neurology is the world's largest association of neurologists and neuroscience professionals, with 36,000 members. The AAN is dedicated to promoting the highest quality patient-centered neurologic care. A neurologist is a doctor with specialized training in diagnosing, treating and managing disorders of the brain and nervous system such as Alzheimer's disease, stroke, migraine, multiple sclerosis, concussion, Parkinson's disease and epilepsy.

Leaving Tiny, Unruptured Intracranial Aneurysms Untreated

You'll want to discuss this with your doctor. Why the recommendation to treat that small aneurysm and cut your life short by two years? 

Leaving Tiny, Unruptured Intracranial Aneurysms Untreated


Why Is It So Hard?

JAMA Neurol. 2018;75(1):13-14. doi:10.1001/jamaneurol.2017.2559
One of the frustrations that drove me back to focusing more on delivery of care and less on research was the difficulty in changing practice with the results of research. Nearly 20 years ago, my research group started to study the question of which intracranial aneurysms should be treated. The results were startling: the vast majority of small, unruptured aneurysms should be left untreated, even if the published evidence was off target by a large margin.1 However, these results had little effect. In spite of 2 decades of largely confirmatory evidence for very small aneurysms (arbitrarily set at ≤3 mm in diameter) showing that coil embolization is not as safe as some believe and that rupture and growth rates are extremely low, many continue to recommend treatment for most of these aneurysms.
The updated analysis produced by Malhotra and colleagues2 in this issue of JAMA Neurology paints the picture very clearly. The best approach for patients with aneurysms measuring 3 mm or less in diameter is to ignore the aneurysms: there is no need for follow-up imaging and certainly no need to try to treat them. Treating very small aneurysms is projected to reduce a person’s healthy lifespan by nearly 2 years. That’s right—you try to treat that little aneurysm and you are likely to knock a couple of years off someone’s life. Could the estimates used in the model change the recommendation? The data would have to be unbelievably wrong to change the recommendation. For example, the annual rupture rate of an untreated aneurysm would need to be more than 1.7% to change the recommendation, and no study has shown a rate close to this, with a best estimate being 0.23%. Furthermore, one can always argue that the underlying studies could be better, but what happened to that oath we all took, “First do no harm…”? With the best estimate suggesting we shorten a patient’s lifespan by 2 years when we treat a very small aneurysm, we should stop treating now rather than waiting for better data to change course.
Perhaps even more remarkable in this analysis is the conclusion that we do more harm than good from monitoring patients with magnetic resonance angiography regardless of whether the duration between scans is 1, 2, or 5 years, and this is without any consideration of cost. It would seem counterintuitive that more monitoring could be harmful when the monitoring itself is completely safe. However, we have seen from prostate-specific antigen testing for prostate cancer that the result of a screening test may worsen health outcomes.3 Monitoring can push us to intervene and these interventions can have negative effects. It is an old story.
I suspect that these results, as with all those before them, will be ignored by some practitioners. I would like to examine several arguments I have heard through the years to justify treating such small aneurysms.
One frequent argument for proceeding with treatment even when the evidence recommends avoiding it is that the potential for the aneurysm to rupture produces anxiety that will affect a patient’s quality of life, making treatment the right decision. However, when it is clear that the risk of rupturing the aneurysm or causing a stroke is greater by treating the aneurysm than leaving it alone, this concern should be reduced. We all know how suggestible patients can be, which makes it even more critical that we carefully educate them, perhaps even scripting the way we introduce the choices. Proper education and counseling are much safer and more appropriate interventions for this anxiety.
Another argument is that the procedural risks used in these models are inflated and do not reflect those at one’s own institution. In fact, the estimates in the models are based on the published literature. Several studies have shown that there is a tendency to underreport adverse outcomes in case series such as these,4 in part related to discomfort in accurately reporting adverse outcomes, so published estimates are probably underestimates. Furthermore, studies have shown that practitioners routinely underestimate their complication rates. The solution here is for physicians to distrust their own intuitions about local institutional complication rates and outcomes. The literature is almost certainly more accurate and should not be ignored. Your results are probably poorer than those published by your colleagues.
Some believe that the fact that many ruptured aneurysms are small means that the only way to prevent rupture is to treat small aneurysms. Although this idea is logical on the surface, it presumes that a static, small aneurysm existed for some number of months or years before rupturing, but the literature does not support that supposition. When we find and follow up small unruptured aneurysms, they almost never grow and almost never rupture. It is possible that the small aneurysms that rupture emerged days or even hours before rupture and that the ones we find incidentally are disproportionately stable. This possibility certainly fits the data.
A final argument I have heard to justify treatment of very small aneurysms is that a particular aneurysm is at high risk for rupture because of its configuration or location, the patient’s family history, history of rupture of a different aneurysm, or some other consideration. Undoubtedly, there are higher-risk tiny aneurysms, and the literature suggests a few such risk factors. However, the overall rates of rupture for tiny aneurysms are extremely low even when these subgroups are included, so these factors are of questionable importance in a given case.
Underlying these arguments are biases working behind the scenes, perhaps even subconsciously. Although we would love to deny it, we physicians are human and humans are by nature subject to an array of biases.
An example of such a bias is optimism. Even the proceduralists with the best skills have cases with complications. Going to work every day requires that they minimize the emotional effect of these complications on themselves. It would be too great a burden to acutely feel a complete sense of responsibility for every avoidable death or disabling complication, particularly in the highly risky and complex area of cerebrovascular disease. Proceduralists must be built to bounce back and move on; however, taken too far, this attitude can create a bias toward underestimating the rate and outcome of these same complications. This bias toward optimism about one’s own outcomes is not universal, of course, and we have all seen both “cowboys” and “turtles,” with the latter representing those we refer to when caution is preferred.
Career advancement is a bias to which we are all subject. For some, the longer the list of treated patients, the more impressive the published case series, and the greater the bragging rights and consequent referral base. Financial incentives also play into treatment decisions more than any of us would like to admit. Whether a physician benefits directly from treating more cases, as in private practice or with similar incentive plans, or benefits indirectly by achieving relative-value units that justify a high salary or bonus, the incentive to do more in our health care system is a very strong one. Physicians, department chairs, and hospitals are all complicit. One way to reduce this bias is to make sure the physicians making the decision about when treatment is necessary are not financially incentivized to do so.
Finally, the bias to do things as they have always been done is powerful in medicine. My generation of stroke physicians was taught that unruptured aneurysms were time bombs that should be identified and defused as soon as possible. It is extremely difficult to unteach that belief, with years of experience and all our trusted colleagues and mentors pushing in the opposite direction. The best solution here is probably to allow for greater coordination of care in multidisciplinary teams, where members keep each other up to date and ensure alignment with the latest and most reliable evidence. Greater devotion to tracking and achieving better outcomes could also help change the calculus to constant evolution toward the best treatment approach.
I hope this updated analysis will change the standard for how we approach tiny unruptured aneurysms. More important, I hope it is also a call to arms for creating a more responsive and responsible system of care that reduces the outcome of our biases and more closely adheres to the interests of the patient. Such a system would reward good outcomes rather than more care, and would include direct, ongoing feedback of outcomes to encourage integration of the best data elsewhere and generate new data in the delivery of care. Given my own frustration with the effect and pace of research, I am moving on to developing that system. Wish me luck. I will need it.
Back to top
Article Information
Corresponding Author: S. Claiborne Johnston, MD, PhD, Dell Medical School, University of Texas at Austin, 1501 Red River, Stop Z0100, Austin, TX 78712 (clay.johnston@austin.utexas.edu).
Published Online: November 20, 2017. doi:10.1001/jamaneurol.2017.2559
Conflict of Interest Disclosures: None reported.

Neurorehabilitation After Stroke From Bedside to the Laboratory and Back

A couple comments on what I can read;

There is no long path to recovery; THERE IS NO FUCKING PATH AT ALL

Predicting recovery is not essential; IT IS A TOTAL FUCKING WASTE OF TIME. 

I can't see the multidisciplinary team being that useful: WITH NO PROTOCOLS EVERYTHING IS JUST GUESSWORK AND HOPE. 

Neurorehabilitation After Stroke - From Bedside to the Laboratory and Back

Originally publishedhttps://doi.org/10.1161/STROKEAHA.118.023878Stroke. ;0

 First page image

Thursday, May 30, 2019

The Role of Antioxidant Treatment in Acute Ischemic Stroke: Past, Present and Future

Maybe our stroke leaders can use this to figure out next steps in the strategy to solve stroke. Or much more likely they will do absolutely nothing. Only 7 pages. 

The Role of Antioxidant Treatment in Acute Ischemic Stroke: Past, Present and Future

Neuroplasticity and practical principles of practice for brain injured patients

Yes, we know neuroplasticity works but all this is practically useless since there is NO EXACT PROTOCOL TO FOLLOW.  Until we know why and how a neuron gives up its current function to take on a neighbors task it will never become usefully repeatable. Principles are not good enough.

Neuroplasticity and practical principles of practice for brain injured patients


 In blogs, Thought Piece

Neuroplasticity is the ability of the brain whether injured or uninjured to learn new behaviours and functions by neurons altering their structure, function and forming neural pathways for the adaption to take place.
This post is going to look at neuroplasticity and its relevance to rehabilitation as well as a summary of the principles of experience-dependent plasticity in rehabilitation. (Kleim and Jones, 2008)
There is significant evidence which indicate that the brain is creating new connections and neural pathways to store new experiences and to allow for behavioural changes. This is a process which is taking place constantly. (Black, Jones, Nelson and Greenough, 1997; Grossman, Churchill, Bates, Kleim and Greenough, 2002).
After a brain injury, learning and re-learning is an essential part of brain adaptation. We often see how the brain re-learns movements by the way the individual develops compensatory behavioural movements to functionally adapt after a brain injury. This can be seen by an individual with hemiplegia (one side affected) being dominant and reliant on the unaffected side. Eg. Weight bearing only on the one leg. The process of rehabilitation looks at correcting these functional maladaptations using neuroplasticity and the principles discussed later in combination with a structured exercise program.
Brain damage changes the way the brain responds to learning. A brain injury not only affects movements but can also affect speech, cognition, mood and we therefore require a multidisciplinary approach to treating individuals with a brain injury.
Principles of experience-dependent plasticity in rehabilitation.
Kleim and Jones (2008), identified 10 principles which hold relevance to outcomes in brain plasticity in the injured and uninjured brain.
  • Use it or lose it

If you had any brains at all you would realize this quantifying nonuse doesn't get survivors recovered at all. Create protocols for 100% recovery and nonuse wouldn't exist. SOLVE THE CORRECT PROBLEM!  I have dead brain there so use of the muscle is impossible; stop blaming me for not recovering! You need to create dead brain rehab protocols!

 
There seems to be functional loss in behavioural movements and patterns if there is no specific training in the functional movements.
  • Use it and improve it
In rehabilitation it is important to understand what the intended outcome of our rehabilitation process is. Plasticity can be induced by training on specific movements and behavioural patterns which can bring about improvements in the task.
  • Specificity
Specificity of the movements is key to bring about the desired plastic changes to the brain.
  • Repetition
Repetition of the specific movements is required to induce lasting changes in the neural circuits for a specific movement or behavioural pattern. With increased repetition we wish to drive long lasting effects so that the skill/movement or behaviour is resistant to decay when there is a period of no stimulus.
  • Intensity
The intensity of the stimulus is important to carry out plastic changes. The greater the intensity of the stimulus the greater the impact of neuroplasticity. A higher number of repetitions of a task as well as it being driven with a great deal of intensity has shown to increase the number of synapses in the motor cortex. (Kleim, Barbay, et al. 2002).
It is important to note with intensity however, there needs to be careful consideration to patients being exposed to overuse injuries using this rule. A clinician should use good judgement as to find the appropriate intensity for the person being treated.
  • Time
The brain is a complex structure and unit and something which we still don’t fully understand as its ability and potential is still being analysed. We can not fix a set time in which we will see neuroplastic changes and say when specific adaptations will occur. We should look at neuroplasticity as a process. We see different adaptations taking place depending on the persons injury and where they are in the rehabilitation process.
  • Salience
The exercise or therapy done needs to be quality in nature. Exercises need to be significant and time needs to be utilised effectively. The person needs to feel that they are important as well, as emotion has a contribution to memory consolidation.
  • Age matters
In the normal brain, with time we are subject to cognitive decline. In the younger individual, the impact of neuroplasticity is much higher, and they can adapt to changes and responses much quicker than the older individual. This does not mean that an older individual with a brain injury will not benefit from therapy, it just means that the timeline for improvement might take a bit longer compared to a younger individual.
  • Transference
Plasticity of developing a skill in one task may have a transfer onto another skill or task. A multidisciplinary approach is important in treating persons with a brain injury as it makes use of this principle and we have experienced this in the rehabilitation setting.
  • Interference
Another principle which highlights the importance of a multidisciplinary approach is interference. Plasticity of developing a skill in one task or behaviour may have a negative impact in another area. Therefore, it is important that we not only highlight and focus on the positive gains, but we also look holistically and notice if there have been any deteriorations in another aspect.
As stated by Kleim and Jones, 2008, this list is not a comprehensive list, but it brings forth keys principles which researchers have found to be relevant to rehabilitation of persons with brain injury. It gives a guideline for individuals who are looking into therapy for themselves or people they know who have had a brain injury and aids clinicians who wish to design and structure their rehabilitation program. As a Biokineticist we aim to use these principles in a structured exercise rehabilitation program to maximise the benefits of therapy for the individual.
References:
Kleim, J.A., Jones, T.A., (2008). Principles of experience dependent neural plasticity: Implications for rehabilitation after brain damage. Journal of Speech, Language, and Hearing Research, 51, 225-239.
Black, J. E., Jones, T. A., Nelson, C. A., & Greenough, W. T. (1997). Neuronal plasticity and the developing brain. In J. D. Noshpitz, N. E. Alessi, J. T. Coyle, S. I. Harrison, & S. Eth (Eds.), Handbook of child and adolescent psychiatry (Vol. 6, pp. 31–53). New York: Wiley.
Grossman, A. W., Churchill, J. D., Bates, K. E., Kleim, J. A., & Greenough, W. T. (2002). A brain adaptation view ofplasticity:Issynapticplasticityanoverlylimitedconcept? Progress in Brain Research, 138, 91–108.
Kleim, J. A., Barbay, S., Cooper, N. R., Hogg, T. M., Reidel,C.N.,Remple,M.S.,etal.(2002).Motorlearningdependent synaptogenesis is localized to functionally reorganized motor cortex. Neurobiology of Learning and Memory, 77, 63–77.

Lower Limb Ischaemic Per-Conditioning Does Not Reduce Final Infarct Size in Patients With Acute Ischemic Stroke

But what about these lower limb interventions? Does your doctor know of them? 

Leg compressions may enhance stroke recovery August 2012

Leg wraps raise hopes of saved lives after strokes May 2013 

Your doctor and hospital not knowing and implementing these easy interventions is the very pinnacle of incompetence.

 

Lower Limb Ischaemic Per-Conditioning Does Not Reduce Final Infarct Size in Patients With Acute Ischemic Stroke

MILAN, Italy -- May 24, 2019 -- In-hospital remote ischaemic per-conditioning (per-CID) within 6 hours is safe, but shows no benefits over sham procedure for patients with confirmed acute ischaemic stroke undergoing thrombolysis, according to a study presented here at the 5th European Stroke Organisation Conference (ESOC).

The findings, presented by Fernando Pico, MD, Versailles Mignot Hospital, Versailles, France, come from the Remote Ischemic Conditioning in Acute Brain Infarction Study (RESCUE-BRAIN) trial.

per-CID was designed to cause transient limb ischaemia to induce ischaemic tolerance and promote endogenous mechanisms to increase cerebral blood flow. per-CID showed a cardioprotective effect in a randomised control trial involving 250 patients within the 6 first hours of myocardial infarction who were candidates for primary angioplasty.

“In cardiology, for myocardial infarction, one study showed that ischaemic conditioning reduces the size of the myocardial lesion,” said Dr. Pico.

Therefore, the researchers wanted to determine whether per-CID in the unaffected lower limb performed within the first 6 hours of cerebral infarction could reduce the growth of the brain infarction.

For the current study, 93 patients with MRI-confirmed carotid ischaemic stroke received a lower limb tourniquet on half of the thigh within 6 hours of symptom onset. The per-conditioning protocol consists of 4 cycles of electronic tourniquet inflation (5 minutes) and deflation (5 minutes) to the thigh over 40 minutes. Another 95 patients had a sham cuff placed. MRI was repeated 24 hours after stroke onset.

Around 90% of patients had been treated with intravenous thrombolysis (median time, 2.5 hours) and about a third had undergone endovascular treatment (median time, 3.2 hours). Median time between stroke onset and cuff inflation was 3.7 hours.

The primary outcome was changes in diffusion-weighted imaging brain infarction volume between baseline and 24 hours.

In the intention-to-treat analysis, there were no significant differences between groups in final infarct size (mean log10 change, 0.37 vs 0.30 and median percentage change in brain infarction volume, 34.1% vs 36.5%).

Similarly, there were no significant differences for secondary endpoints of change in NIHSS score at 24 hours, 90-day Bathel ≥95, and 90-day modified Rankin score 0-1.

“RESCUE BRAIN is a neutral randomised controlled trial, with no benefit, but not harmful,” said Dr. Pico.

[Presentation title: A French Multicenter Randomized Trial on Neuroprotection With Lower Limb Ischemic Per-Conditioning in the Acute Phase of Cerebral Infarction]

Robot-Assisted Training Does Not Improve Upper Limb Function After Stroke

A 44% success rate would assuredly be good enough for most stroke patients to try it.  Using the Action Research Arm Test for validation is not useful, it is subjective.  And did you also not consider that the therapy repetitions was not enough? I suggest you analyze why it didn't meet your criteria and try again. Survivors try movements millions of times and still don't give up. Why do you give up after 1 try?

Robot-Assisted Training Does Not Improve Upper Limb Function After Stroke

MILAN, Italy -- May 27, 2019 -- Robot-assisted training of the upper limb does not improve upper limb function, compared with usual care, for patients with moderate or severe upper limb functional limitation after a stroke, according to a study presented here at the 5th European Stroke Organisation Conference (ESOC).

“Loss of arm function is a common problem after stroke,” reported Helen Rodgers, MD, Stroke Research Group, Newcastle University, Newcastle upon Tyne, United Kingdom, and colleagues. “We compared the clinical effectiveness of robot-assisted training using the MIT-Manus robotic gym with an enhanced upper limb therapy programme based on repetitive functional task practice and with usual care.”

Between April 14, 2014, and April 30, 2018, 770 patients who experienced a stroke were randomised to either robot-assisted training (n = 257), an enhanced upper limb therapy programme (n = 259), or usual care (n = 254).

The robotic gym system and EULT was delivered for 45 minutes, 3 times per week for 12 weeks.

The primary outcome of upper limb function success -- defined using the Action Research Arm Test (ARAT) at 3 months -- was achieved by 103 (44%) of 232 patients in the robot-assisted training group, by 118 (50%) of 234 patients in the EULT group, and by 85 (42%) of the 203 patients in the usual care group.

Compared with usual care, robot-assisted training (adjusted odds ratio [aOR] = 1.17; 98.3% confidence interval [CI], 0.70-1.96) and EULT (aOR = 1.51; 98.3% CI, 0.90-2.51) did not improve upper limb function, and the effects of robot-assisted training did not differ from EULT (aOR = 0.78; 98.3% CI, 0.48-1.27).

More participants in the robot-assisted training group and EULT group had serious adverse events than in the usual care group, but none were attributable to the intervention.

“[The] results [of RATULS] do not support the use of robot-assisted training as provided in this trial in routine clinical practice,” the authors concluded

[Presentation title: A Multi-Centre Randomised Controlled Trial Comparing: Robot-Assisted Training: an Enhanced Upper Limb Therapy Programme and Usual Care]

A 10 minute Stroke Research Register Survey - Hunter Medical Research Institute, Australia

I answered this because the same needs exist all over the world. I told them to work on the neuronal cascade of death and stop calling it neuroprotection which doesn't give any sense of urgency. 

Hunter Medical Research Institute, Australia

Chronic Cortical Cerebral Microinfarcts Slow Down Cognitive Recovery After Acute Ischemic Stroke

Survivors don't give a shit about predicting slower cognitive speed. They want interventions that prevent that.  Have you never talked to stroke survivors about why you are doing research and how it will help their recovery?

Chronic Cortical Cerebral Microinfarcts Slow Down Cognitive Recovery After Acute Ischemic Stroke

Originally publishedhttps://doi.org/10.1161/STROKEAHA.118.024672Stroke. 2019;50:1430–1436

Background and Purpose—

Cortical cerebral microinfarcts (CMIs) have been associated with vascular dementia and Alzheimer disease. The aim of the present study was to evaluate the role of cortical CMI detected on 3T magnetic resonance imaging, on the evolution of cognition during the year following an acute ischemic stroke.

Methods—

We conducted a prospective and monocentric study, including patients diagnosed for a supratentorial ischemic stroke with a National Institutes of Health Stroke Scale score ≥1, without prestroke dementia or neurological disability. Cortical CMIs were assessed on a brain 3T magnetic resonance imaging realized at baseline, as well as markers of small vessel disease, stroke characteristics, and hippocampal atrophy. Cognitive assessment was performed at 3 time points (baseline, 3 months, and 1 year) using the Montreal Cognitive Assessment, the Isaacs set test, and the Zazzo’s cancellation task. Generalized linear mixed models were performed to evaluate the relationships between the number of cortical CMI and changes in cognitive scores over 1 year.

Results—

Among 199 patients (65±13 years old, 68% men), 88 (44%) had at least one cortical CMI. Hypertension was the main predictor of a higher cortical CMI load (B=0.58, P=0.005). The number of cortical CMI was associated with an increase time at the Zazzo’s cancellation task over 1 year (B=3.84, P=0.01), regardless of the other magnetic resonance imaging markers, stroke severity, and demographic factors.

Conclusions—

Cortical CMIs are additional magnetic resonance imaging markers of poorer processing speed after ischemic stroke. These results indicate that a high load of cortical CMI in patients with stroke can be considered as a cerebral frailty condition which counteracts to the recovery process, suggesting a reduced brain plasticity among these patients.

Footnotes

The online-only Data Supplement is available with this article at https://www.ahajournals.org/doi/suppl/10.1161/STROKEAHA.118.024672.
Correspondence to Sharmila Sagnier, MD, INCIA-UMR 5287-Université Bordeaux 2, 146 rue Léo Saignat Zone Nord, Bâtiment 2A 2e étage, 33076 Bordeaux Cedex, France. Email

Wednesday, May 29, 2019

Association of stroke among adults aged 18 to 49 years with long-term mortality

I just miss qualifying as a young adult, had my stroke at age 50 thirteen years ago. I'm going to live for a good long time yet, drinking wine and beer and doing stuff that any doctor would tell me was not ok. 

Association of stroke among adults aged 18 to 49 years with long-term mortality

JAMAEkker MS, et al. | May 28, 2019
Researchers performed this Dutch register-based cohort study to determine the age- and sex-specific case fatality and long-term mortality associated with stroke among young adults. This study included 15,527 patients who had the first stroke between the ages 18 of 49 years in 1998-2010; they were followed up until January 1, 2017. Observations revealed that young adults who were 30-day survivors, continuously have elevated mortality risk up to 15 years after stroke.


Methods

  • The investigators identified patients and outcomes via linking the national Hospital Discharge Registry, national Cause of Death Registry, and the Dutch Population Register.
  • Exposures included first stroke occurring between the ages of 18 to 49 years, which were documented using International Classification of Diseases, Ninth Revision, and International Statistical Classification of Diseases and Related Health Problems, Tenth Revision, codes for ischemic stroke, intracerebral hemorrhage, and stroke not otherwise specified.
  • As the primary outcome, 30-day survivors at end of follow-up were assessed for all-cause cumulative mortality stratified by age, sex, and stroke subtype.
  • Comparison to all-cause cumulative mortality in the general population was also done.

Results

  • At end of follow-up, over 3,500 cumulative deaths were reported, including 1,776 deaths within 30 days post-stroke and 1,764 deaths during a median duration of follow-up of 9.3 years
  • The 15-year mortality in 30-day survivors was 17.0% (95% CI: 16.2% to 17.9%).
  • Compared with the general population, the standardized mortality rate was 5.1 for ischemic stroke, and the standardized mortality rate for intracerebral hemorrhage was 8.4.(Whatever the hell this means, obviously not meant for lay persons.)
Read the full article on JAMA

 

How a fruit compound may lower blood pressure - resveratrol

I'm doing it the wine way, although I have no idea of the amount that I need to drink. You won't get an answer from your doctor on that question. Alcohol is never an answer for them. Don't try this on your own, you have no clue how to translate mice body size and amount of resveratrol to human size and then convert that to bottles of red wine. Or you could wait for this tomato to be created. Social connections wouldn't be the same over tomatoes.

Scientists Produce Beneficial Natural Compounds In Tomato - Industrial Scale Up Potential, resveratrol and Genistein

How a fruit compound may lower blood pressure - resveratrol

Healthline/Medical News Today | May 28, 2019
Blueberries, red grapes, red wine, and peanuts are some of the natural sources of resveratrol—a plant compound that has received much attention in the medical community recently. New research in mice and human cells breaks down the mechanism through which resveratrol may lower blood pressure.
Advertisement
From protecting our neurons against aging to potentially preventing cancer, a significant number of studies have recently hailed the health benefits of resveratrol. Also, a lot of previous research has focused on the benefits of resveratrol for heart health. Clinical studies in rats and mice have demonstrated protective effects against stroke, heart failure, and hypertension, among other heart conditions.
Although some researchers believe that the benefits of resveratrol come from its antioxidant properties, the mechanisms behind its cardioprotective effects remain unclear. New research gets closer to understanding these mechanisms, and the findings are an intriguing paradox.
A team of scientists from King's College London (KCL), in the United Kingdom, added resveratrol to the diet of mice with high blood pressure. Joseph Burgoyne, PhD, a senior lecturer in cardiovascular sciences at KCL, is the lead author of the study, which appears in the journal Circulation.

The effects of resveratrol in mice

Burgoyne and the team induced high blood pressure in a group of wild-type mice. The researchers measured the rodents' blood pressure with implanted telemetry probes and monitored it for 15 days. During this time, they fed the mice either a diet to which they had added resveratrol or a normal diet.
By the end of the study period, the researchers noted a drop of about 20 millimeters of mercury in the blood pressure of mice that had consumed resveratrol. The scientists also discovered that resveratrol relaxed the rodents' blood vessels by oxidizing the protein PKG1a.
"Resveratrol mediates lowering of blood pressure by paradoxically inducing protein oxidation, especially during times of oxidative stress, a mechanism that may be a common feature of 'antioxidant' molecules," conclude the authors.
The findings are counterintuitive, in the sense that the compound is believed to be an antioxidant, but this study shows that it behaves like an oxidant in order to lower blood pressure.
"We're slowly realizing that oxidants aren't always the villain. Our research shows that a molecule once deemed an antioxidant exerts its beneficial effects through oxidation. We think that many other so-called 'antioxidants' might also work in this way."
—Joseph Burgoyne, PhD

What do the findings mean for humans?

Importantly, the researchers were able to replicate the findings in human cell lines. Specifically, they applied resveratrol to smooth muscle cells taken from human blood vessels and noticed the same oxidization process. However, the scientists caution against the interpretation that people should consume a lot of resveratrol-containing products in order to reap the same benefits that this study showcased in mice.
People should avoid red wine, in particular, the researchers warn. To recreate the benefits of the study in humans, say Burgoyne and colleagues, a person would have to consume 1,000 bottles of red wine every day. The compound is not very soluble, which is why high amounts of it are necessary.
"Our work could lay the foundations for chemically altering resveratrol to improve its delivery to the body," the study's lead author explains, "or designing new, more potent drugs which use the same pathway. In the future, we could have a whole new class of blood pressure drugs."
Metin Avkiran, PhD, a professor of molecular cardiology at KCL—who was not involved in the study—also comments on the significance of the findings.
"Unfortunately, this isn't the all-clear to open a bottle of merlot. To get the human equivalent dose of resveratrol used here, you'd need to drink an impossible amount of red wine every day."
—Professor Metin Avkiran, PhD
"This study reveals the surprising way in which resveratrol works and opens up the possibility of new blood pressure drugs which work in a similar way," Avkiran adds. "The findings bring us a step closer to tackling this 'silent killer' which puts people at risk of having a devastating stroke or heart attack."
In the United States, over 100 million people are currently living with hypertension.
To read more, click here.

Memantine Improves Lewy Body Dementia & Parkinson's

You might want to remember this because of your chance of getting Parkinsons.

Parkinson’s Disease May Have Link to Stroke March 2017

 

Memantine Improves Lewy Body Dementia & Parkinson's 

Memantine (Namenda / Ebixa) is FDA-approved for Alzheimer's. Learn how it significantly improves memory and attention in Lewy Body Disease, Parkinson's and various types of dementia.



An important study shows that performance on objective tests of attention and memory can be improved by memantine in two other major forms of dementia - Parkinson's disease dementia and dementia with Lewy Bodies. The improvements detected were highly statistically reliable and of clinically relevant effect sizes; indicating that memantine can produce cognitive benefits in patients with these dementias which match those seen previously with anticholinesterases.

Memantine is FDA approved just for Alzheimer's. Doctors may prescribe it "off-label", if in their clinical judgment it may help their patient with Lewy Body dementia or Parkinson's disease.

Both studies utilised the CDR System™, an automated cognitive test system, making a strong case for benefits for the increased sensitivity and specificity that such procedures bring to dementia research, when compared with the traditional tests which have been historically employed.

The results were part of a presentation at the last Alzheimer's Association International Conference.

The current consensus guidelines for diagnosis of dementia with Lewy Bodies (DLB) and Parkinson's disease dementia (PDD) identify deficits to attention as core features in both conditions. (2,3). The present study evaluated the effects of memantine in DLB & PDD.

In related trials to date in both dementias, the CDR System has detected significant benefits with rivastigmine on various aspects of attention (4-7).

METHODS

  1. This was a parallel group, double-blind, placebo controlled, multicentre trial of memantine
  2. 21 DLB and 30 PDD patients were assessed prior to dosing and again at 12 and 24 weeks
  3. CDR System tests of attention (simple and choice reaction time) and word recognition (immediate and delayed) were administered.
  4. The tasks were secondary measures and not included in the original study publication (8).

RESULTS

  • Compared to placebo, memantine significantly improved choice reaction time (CRT) and the accuracy of both immediate and delayed word recognition (all p<0.02); with Cohen's d effect sizes of between 0.56 and 0.57.
  • The improvement in CRT was accompanied by a trend for improved accuracy on the task, and speed was numerically improved with memantine on the word recognition tasks.
  • Beneficial effects of memantine were seen on 3 of the 4 tasks used in this study.

These are the first therapeutic improvements with memantine having clinically relevant effect sizes in either DLB or PDD on validated automated cognitive tests of attention and episodic recognition memory. They directly support the improvement in the primary study outcome. Every measure from every CDR System test moved in the direction of improvement with memantine.

The analysis models included a term for the interaction between type of dementia with effects of treatment, but none of these approached significance for any measure. Thus the improvements with memantine occurred in both DLB and PDD.

REFERENCES
1.
Ballard CG, Aarsland D, McKeith IG et al. Fluctuations in attention: PD dementia vs. DLB with Parkinsonism. Neurology 2002; 59: 1714-1720.
2.
McKeith IG, Dickson DW, Lowe J. Diagnosis and management of dementia with Lewy bodies: Third report of the DLB consortium. Neurology 2005; 65: 1863–1872.
3.
Emre M, Aarsland D, Brown R et al. Clinical Diagnostic Criteria for Dementia Associated with Parkinson's Disease. Movement Disorders 2007; 22: 1689-1707.
4.
McKeith IG, Del Ser T, Spano P, et al. Efficacy of rivastigmine in dementia with Lewy bodies: a randomised, double-blind, placebo-controlled international study. Lancet 2000; 356: 2031-2036.
5.
Wesnes KA, McKeith IG, Ferrara R et al. Effects of rivastigmine on cognitive function in dementia with Lewy bodies: a randomised placebo-controlled international study using the Cognitive Drug Research computerised assessment System. Dementia and Geriatric Cognitive Disorders 2002; 13: 183-192.
6.
Emre M, Aarsland D, Albanese A et al. Rivastigmine for dementia associated with Parkinson's disease. The New England Journal of Medicine 2004; 351: 2509-2518.
7.
Wesnes KA, McKeith IG, Edgar C et al. Benefits of rivastigmine on attention in dementia associated with Parkinson disease. Neurology 2005; 65: 1654-1656.
8.
Aarsland D, Ballard C, Walker Z et al. Memantine in patients with Parkinson's disease dementia or dementia with Lewy bodies: a double-blind, placebo-controlled, multicentre trial. Lancet Neurology 2009; 8: 613–618.

At baseline, compared to healthy age-matched controls the patients showed the previously identified characteristic profile of attentional impairment; as well as large effect sized deficits to CRT and the recognition accuracy scores.