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:

Wednesday, August 24, 2016

Scientists use ultrasound to jump-start a man's brain after coma

We'll never know if this might be useful for locked in syndrome because we have NO stroke leader to talk to or any stroke strategy to update.

A 25-year-old man recovering from a coma has made remarkable progress following a treatment at UCLA to jump-start his brain using ultrasound. The technique uses sonic stimulation to excite the neurons in the thalamus, an egg-shaped structure that serves as the brain's central hub for processing information.
"It's almost as if we were jump-starting the neurons back into function," said Martin Monti, the study's lead author and a UCLA associate professor of psychology and neurosurgery. "Until now, the only way to achieve this was a risky surgical procedure known as , in which electrodes are implanted directly inside the thalamus," he said. "Our approach directly targets the thalamus but is noninvasive."
Monti said the researchers expected the positive result, but he cautioned that the procedure requires further study on additional patients before they determine whether it could be used consistently to help other people recovering from comas.
"It is possible that we were just very lucky and happened to have stimulated the patient just as he was spontaneously recovering," Monti said.
A report on the treatment is published in the journal Brain Stimulation. This is the first time the approach has been used to treat .
The technique, called low-intensity focused ultrasound pulsation, was pioneered by Alexander Bystritsky, a UCLA professor of psychiatry and biobehavioral sciences in the Semel Institute for Neuroscience and Human Behavior and a co-author of the study. Bystritsky is also a founder of Brainsonix, a Sherman Oaks, California-based company that provided the device the researchers used in the study.
That device, about the size of a coffee cup saucer, creates a small sphere of acoustic energy that can be aimed at different regions of the brain to excite tissue. For the new study, researchers placed it by the side of the man's head and activated it 10 times for 30 seconds each, in a 10-minute period.
Monti said the device is safe because it emits only a small amount of energy—less than a conventional Doppler ultrasound.
Before the procedure began, the man showed only minimal signs of being conscious and of understanding speech—for example, he could perform small, limited movements when asked. By the day after the treatment, his responses had improved measurably. Three days later, the patient had regained full consciousness and full language comprehension, and he could reliably communicate by nodding his head "yes" or shaking his head "no." He even made a fist-bump gesture to say goodbye to one of his doctors.
"The changes were remarkable," Monti said.
The technique targets the thalamus because, in people whose mental function is deeply impaired after a coma, thalamus performance is typically diminished. And medications that are commonly prescribed to people who are coming out of a coma target the only indirectly.
Under the direction of Paul Vespa, a UCLA professor of neurology and neurosurgery at the David Geffen School of Medicine at UCLA, the researchers plan to test the procedure on several more people beginning this fall at the Ronald Reagan UCLA Medical Center. Those tests will be conducted in partnership with the UCLA Brain Injury Research Center and funded in part by the Dana Foundation and the Tiny Blue Dot Foundation.
If the technology helps other people recovering from coma, Monti said, it could eventually be used to build a portable device—perhaps incorporated into a helmet—as a low-cost way to help "wake up" patients, perhaps even those who are in a vegetative or . Currently, there is almost no effective treatment for such patients, he said.

Biomarkers May Help Predict Ischemic Stroke Risk

Anything in here that tests for stiff arteries?  What about for hemorrhagic strokes?
Patients with high levels of four blood biomarkers may be more likely to have an ischemic stroke than those with low rates of the markers, researchers reported.
In an observational study, natural logarithmic statistical transformation of markers of inflammatory, endothelial, and oxidative stress – C-reactive protein (CRP), tumor necrosis factor 2 (TNF2), total homocysteine (tHcy), and vascular endothelial growth factor (VEGF) – were each tied to a greater risk of incident ischemic stroke, Ashkan Shoamanesh, MD, of McMaster University, and colleagues reported online in Neurology.
"Identification of persons at high risk of stroke allows for development of targeted interventions to reduce the burden of stroke at the individual and population levels," study co-author Jose Romero, MD, of Boston University, told MedPage Today.
Using the biomarkers also helped better predict the risk of a stroke over the more traditionally used Framingham Stroke Risk Study, Romero said.
However, given that the study was observational, the results don't mean that elevation of these markers causes strokes, "nor do we provide thresholds for clinicians to consider increased risk," Romero noted.
Additionally, while the study doesn't suggest that these markers should be measured routinely in clinical practice, it does shed light on additional markers to identify those at a greater risk of a stroke, he said.
For their study, the researchers measured the levels of 15 biomarkers associated with inflammation in the blood of those from the Framingham Heart Study Offspring Cohort who'd never had a stroke. The 3,224 participants averaged 61 years of age at the study's onset and were observed for an average of nine years. During that period, 98 had a stroke.
In a model adjusted for age and sex, four of the 15 biomarkers were linked to an increased stroke risk, they found:
  • CRP: HR 1.28, 95% CI 1.04 to 1.56
  • TNFR2: HR 1.33, 95% CI 1.09 to 1.63
  • tHcy: HR 1.32, 95% CI 1.11 to 1.58
  • VEGF: HR 1.25, 95% CI 1.07 to 1.46
Three of the biomarkers remained significantly associated with stroke risk in a model adjusted for systolic blood pressure, hypertension treatment, current smoking, diabetes, cardiovascular disease, and atrial fibrillation. Only CRP was no longer significant, the researchers said.
Adding the four biomarkers to the Framingham Stroke Risk Profile improved the ability to predict which patients would be at greatest risk for ischemic stroke, they reported.
They also found in exploratory analyses a significant relationship between CRP and a subtype of ischemic stroke: atherosclerotic brain infarction (HR 1.31, 95% CI 1.06 to 1.33). They also saw a relationship between cerebral embolism and both interleukin 6 (HR 1.11, 95% CI 1.06 to 1.33) and fibrinogen (HR 1.40, 95% CI 1.06 to 1.86).
The study was limited by the fact that conditions that may affect vascular and systemic inflammation, such as chronic inflammatory diseases and infections, and long-term use of medications that have anti-inflammatory properties, were unaccounted for. Also, the biomarkers were measured at single time points and not repeated over time, the researchers said.
Deepak Gulati, MD, of the Ohio State University who wasn't involved in the study, called it "preliminary" in terms of establishing any solid evidence of an association between the biomarkers and ischemic stroke, but said it "brings about this important concept that needs to be explored further."
Gulati said that biomarkers must be accurately and reproducibly measurable, clinically feasible, cost effective, and prospectively validated in randomized clinical trials.
"Biomarkers are interesting, but nothing has yet been validated in terms of an ischemic stroke," he said.
Romero said future research could abet the development of "clinically meaningful thresholds" that may be used in practice and the testing of treatments and drugs in clinical trials that incorporate these markers to assess their benefit in treatment decisions for stroke risk reduction.
In an accompanying editorial, Stephen Williams, PhD, of the University of Virginia, and Svetlana Lorenzano, MD, PhD, of Sapienza University in Rome, agreed that the study "helped refine a well-established stroke risk clinical model ... and helped enhance individual stroke risk prediction," but similarly cautioned that it "should be further assessed in prospective investigations."
As of now, added Romero, stroke prevention should continue to focus on the assessment and treatment of modifiable risk factors as suggested by current stroke prevention guidelines.
Neither the researchers nor the editorialists reported any financial relationships with industry.

Nominate someone for this year’s RAISE (Raising Awareness in Stroke Excellence) Awards is Aug. 31.

Another almost completely useless NSA creation. It should be called Raising Awareness in Stroke Failures that the NSA will ignore. RAISF. That would be useful.
Dear dean,
Deadline for nominations is August 31
Nominate Now Arrow
The deadline for making a nomination for this year’s RAISE (Raising Awareness in Stroke Excellence) Awards is Aug. 31.
Over the past six years, National Stroke Association has recognized the efforts of individuals and groups who work to raise awareness for stroke. It’s not too late to nominate someone and recognize their hard work. Learn more about the six categories now.
In health,
signed by Anna Taylor
Anna Taylor, MS
Director, Programs

9707 E. Easter Lane · Suite B
Centennial, CO 80112
1-800-STROKES (787-6537)

Injecting omega-3 fatty acid reduces brain damage in neonatal mouse model of stroke

Could our researchers correlate this research with pre and post treatment using Omega-3s? Who can take this simple task on? Or will this fall thru the cracks like every other interesting stroke study?

Looking at pretreatment with fish oil or post-treatment with fish oil

Injecting omega-3 fatty acid reduces brain damage in neonatal mouse model of stroke
Researchers from Columbia University Medical Center (CUMC) found that omega-3 fatty acids reduced brain damage in a neonatal mouse model of stroke.
Findings from the study were published recently in PLOS ONE.
The researchers treated 10-day-old mice that had incurred hypoxic-ischemic brain injury (caused by a decrease in blood flow and oxygen to the brain, as occurs during a stroke) with a fat emulsion containing either DHA or EPA--omega-3 fatty acids that are found in certain foods and in supplements. The researchers evaluated the mice's neurological function 24 hours and 8 to 9 weeks after the brain injury.
EPA and DHA are bioactive omega-3 fatty acids that are found in oils extracted from cold-water fish. The CUMC researchers and other scientists have shown that these fish-oil fatty acids protect organs and cells in numerous ways after oxygen deprivation, reducing inflammation and cell death.
At 24 hours, mice treated with DHA, but not EPA, had a significant reduction in brain injury. In the following weeks, the DHA group also had significantly better results in multiple brain functions compared to the EPA-treated mice and untreated (control) mice.
The researchers also discovered that these mice had increased concentrations of DHA in their brain mitochondria, energy-producing structures in cells that can be injured by free radicals when blood flow is restored to the brain after a stroke. This process, known as reperfusion injury, is a common cause of brain damage following the oxygen and nutrient deprivation that occurs after a stroke.
"Our findings suggest that injecting the omega-3 fatty acid DHA after a stroke-like event has the ability to protect brain mitochondria against the damaging effects of free radicals," said senior co-author, Vadim S. Ten, MD, PhD, associate professor of pediatrics at CUMC.
Interruption of blood flow and oxygen supply to the brain during or shortly after birth is a major cause of brain damage in newborns, causing life-long neurological impairments in more than 25 percent of those affected. Many of the pathways involved in this type of brain damage are similar to those in an adult stroke.
"Clinical trials are needed to determine if administering lipid emulsions containing DHA shortly after a stroke-like brain injury offers the same neuroprotective effects in babies and adults, as seen in mice. If successful, such trials could lead to the development of a novel therapy for stroke in newborns, children, and adults, addressing a major medical need," said senior co-author Richard J. Deckelbaum, MD, CM, the Robert R. Williams Professor of Nutrition (in Pediatrics) and Professor of Epidemiology and director of the Institute of Nutrition at CUMC.
Columbia University Medical Center

Elevator buttons

Trying to push them when no one else is around. I have to get within one foot of the button, I can rotate my left hand outward that much and as long as the button is around waist height I can get one of my knuckles to push the button, assuming that the buttons aren't in too much of a depression.  The sixth floor button is too high to successfully get most of the time. This is a slow process, but then everything in stroke rehab is slow.

Intravenous glyburide treatment may reduce dangerous brain swelling after stroke

First written about in Jan. 2012. I bet it will take another dozen years before it possibly gets to clinical treatment. With some actual stroke leadership we could get this done much faster, but hey, it is only stroke survivors being impacted, not anyone from the stroke medical world. And this is only a small percent so no big deal.

Exciting Data from Remedy Pharmaceutical-Sponsored Stroke Drug Trial to Be Presented at the 2012 International Stroke Conference in New Orleans

 The latest here:

Intravenous glyburide treatment may reduce dangerous brain swelling after stroke

A phase 2 clinical trial of a drug that may alleviate brain swelling—a dangerous stroke complication—suggests the treatment may help reduce brain injury and death, and information from the study will help design the phase 3 trial. While the trial did not meet its prespecified primary objective, as described in a paper receiving online release in The Lancet Neurology, it did provide additional evidence that intravenous glyburide treatment may improve patient outcomes.
"Although a follow-up clinical study is needed to confirm our preliminary finding, this is the first time a drug has been tested to prevent swelling after a major ," says W. Taylor Kimberly, MD, PhD, of the Massachusetts General Hospital (MGH) Department of Neurology, co-corresponding author of the report. "We believe that glyburide treatment may be an important strategy to minimize injury resulting from brain swelling."
Strokes caused by blockage of the blood supply to a large area of the brain can lead to the accumulation of fluids called edema, causing brain tissue to swell. Since the brain is confined with the skull, significant swelling and the resulting increased pressure can push brain structures out of their normal position, leading to a 50 percent mortality rate for this complication. Treatment with drugs designed to draw fluids out of the brain have had limited effectiveness, and hemicraniectomy—surgical removal of a portion of the skull to allow to swell freely—is not appropriate for all patients and carries its own risk of complications.
Previous studies in animal models of stroke have suggested that glyburide—a drug used to treat type 2 diabetes - might prevent brain swelling in stroke patients. A pilot study led by Kimberly and his co-corresponding author Kevin Sheth, MD, Department of Neurology, Yale University School of Medicine, indicated that glyburide treatment was safe for and led to the phase 2 trial, sponsored by Remedy Pharmaceuticals. Conducted at 18 hospitals across the U.S., the study - entitled the Glyburide Advantage in Malignant Edema and Stoke (GAMES-RP) trial—enrolled 77 patients with strokes affecting one-third or more of a brain hemisphere. Participants were randomly assigned to continuous intravenous treatment with either glyburide or a placebo for a total of 72 hours.
The prespecified primary endpoint of the study was the proportion of patients who, 90 days after their stroke, achieved scores of 0 to 4 on a standardized stroke scale—a range extending from no symptoms to moderately severe disability - without surgery to relieve brain swelling. While around 40 percent of those in each group met those criteria, the authors note that the decision to have surgery was made by the physicians caring for each patient and may have been arrived at more often at some sites than at others.
"Deciding to proceed to a hemicraniectomy is complicated and depends on the judgment of the stroke neurologist, of the neurosurgeon, and the wishes of patients or their families," says Sheth. "This led to variation in practice across the sites, which is appropriate for clinical care but not ideal for the endpoint of a clinical trial; and we believe this is the main reason the primary endpoint was not reached."
The results for other endpoints, however, were more promising - particularly the brain imaging measure of midline shift, which reflects the extent to which brain structures are pressed out of place by brain swelling. "The degree of midline shift was reduced about 40 percent in patients treated with glyburide, and there was a similar reduction in levels of MMP-9, a biomarker that previous studies have associated with after stroke," says Kimberly. "From a clinical standpoint, there was a 50 percent reduction in mortality and a promising trend towards better functional outcome at 90 days." The results of this study are being used to design the phase 3 trial, which will begin enrolling in 2017.
More information: The Lancet Neurology, DOI: 10.1016/S1474-4422

Journal reference: Lancet Neurology search and more info website
Provided by: Massachusetts General Hospital search and more info website

Circadian rhythms and sleep loss: what happens in your brain when you pull an all-nighter?

This is what happened to me when I entered the hospital Sunday morning at 8am and didn't actually sleep until Thursday night due to all the activity in the ER and stepdown units I was in. I remember falling asleep listening to a therapist talk to me on Thursday afternoon trying to get me to perform some task. I failed at what day it was, which was a stupid question to ask. What is your doctors sleep protocol to make sure you are rested and able to consolidate the memories of your therapies?
Ever wondered what happens inside your brain when you stay awake for a day, a night and another day, before you finally go to sleep? Well, we just found out.
It has been known for many years that how sleepy we are, how well we can add up numbers, pay attention or conduct a working memory task depends on how long we have been awake and the time of day. Typically if we stay awake over a period of two days (a day, a night and then the next day) the first 16 hours or so is of wakefulness – performance is good and doesn’t change much.
But then, as we enter the “biological night time”, as indicated by a rise of the hormone melatonin, performance deteriorates rapidly and reaches a minimum at around 6-8am the following morning. On the second day, performance can get a little better (but still well below that of day one) and only returns to normal, baseline levels after a good night’s sleep.
The key characteristic of this performance timeline is that it doesn’t deteriorate linearly based on how long you’ve been awake but is instead modulated by the time of day. In fact, we know now that it isn’t actually “time of day” but “internal biological time of day” that causes the effects of sleep loss. At the behavioural level, then, brain function is determined by the combined effects of circadian rhythmicity and sleep homeostasis – the sleep pressure that builds up during wakefulness and dissipates during sleep.

Circadian rhythm

Circadian rhythmicity can be observed in many aspects of behaviour and physiology and is generated by circadian clocks in nearly every cell in the brain and body. Locally, these rhythms are generated by a feedback loop of clock proteins onto clock genes that express genetic information that is then translated into proteins.

All these clocks – including brain clocks – are synchronised by a central director/conductor located in a brain area called the suprachiasmatic nucleus in the hypothalamus. This area of the brain also drives the rhythm of melatonin in blood and saliva.
So how does this combined action of circadian rhythmicity and sleep homeostasis work? Well, during the biological day the circadian clock generates an alerting or wakefulness promoting signal that becomes stronger as the day progresses and reaches maximum strength in the evening. This may seem a bit paradoxical, but this signal needs to become stronger as the day progresses because sleep pressure also increases the longer we’re awake – so something needs to keep us alert.
But as we enter the biological night, the wakefulness promoting circadian signal dissipates and turns into a sleep promoting signal with a maximum strength at around 6-8am. Again, this may seem a bit paradoxical but under normal conditions when we sleep at night, this comes in handy because the sleep promoting signal allows us to continue to sleep well even after six or seven hours when the sleep pressure has dissipated.
Problems arise when we stay awake at night and the next day, however. During the night, sleep pressure remains high and even increases because we are awake. The circadian signal no longer opposes this pressure and we struggle to stay awake and to perform. The next day, the circadian clock, which still ticks whether we are asleep or not, starts promoting awake signals again so it becomes a little bit easier to perform and stay awake.

What does this look like in the brain?

This is all fine and good and makes sense. Indeed, this working model is widely accepted from what we’ve seen happen when it comes to behaviour. But what does this combined action of circadian rhythm and sleep homeostasis look like within the human brain?

Our team of researchers, from the University of Liege and the University of Surrey, scanned the brains of 33 people using functional magnetic resonance imaging (fMRI) – which gives a detailed picture of levels of neuronal activity throughout the brain – who were sleep deprived over two days and following a period of recovery sleep. We also measured melatonin levels to have a good indicator of internal biological time, which varies between individuals. Our results are published in Science.
For each participant, 13 brain images were obtained while they were conducting a simple reaction time task. Twelve brain images were collected during the sleep deprivation at times characterised by those rapid changes previously observed for performance in the evening and in the morning. The thirteenth image was taken after recovery sleep.
Activity in several brain regions, and in particular subcortical areas (such as the thalamus, a major centre for relaying information to the cortex), followed a 24-hour rhythmic (circadian) pattern the timing of which, surprisingly, varied across brain regions. Other brain regions – in particular frontal brain areas including higher-order association areas – showed a reduction in activity with time awake followed by a return to pre-sleep deprivation levels after recovery sleep. Some brain regions displayed a pattern which was a combination of a rhythmic pattern and a decline associated with time awake.
Even more surprising, these effects of sleep loss on brain activity were much more widespread when the participants performed a simple reaction time task compared to a more complex memory-reliant task.
What all this means is that various brain regions appear to be differently affected by sleep loss and the circadian rhythm, and overall the results demonstrate both the pervasiveness of these effects, but also the similarity and local nature of these influences.

The variety in brain responses shows just how complex the mechanisms are by which the brain responds to sleep loss. It helps us to understand how the brain might maintain performance during the day and night. These results may reassure shift workers and people working very long hours struggling to pay attention and concentrate on their job, particularly in the early morning hours. Yes, your brain is going to be different at night than during the day. They also suggest that if you’re working late, it might be better to wrap it up, get some sleep and start again in the morning.
It may even help us to better understand why many symptoms in psychiatric and neurodegenerative conditions wax and wane, and why in the early morning after a night without sleep we struggle to maintain attention, whereas in the evening it is not an issue.

Medical errors persist, despite increased scrutiny

These are just the explicit errors. They aren't even counting all the omission errors, like the 90% of stroke patients that don't get to full recovery or the 88% of the time tPA doesn't work to fully reverse the stroke. This amounts to completely fudging the numbers. By not reporting on those problems nobody will attempt to fix them. Stroke survivors once again getting screwed because of incompetence. And there are no consequences to the stroke department head for those failures.
Preventable medical errors reported by full-service hospitals in Massachusetts grew 60 percent last year, a rise partly attributed to problems detected in a single hospital’s dialysis unit.
Hospitals disclosed 1,313 errors that harmed or threatened patients in 2015, including 26 cases when the wrong surgery or procedure was done on a patient; 51 instances when a medication error seriously injured or killed a patient; and 446 cases of contaminated drugs, devices, or biologics.
This last category, which accounted for only 37 reports in 2014, constituted most of the overall increase in reported errors.
Baystate Medical Center in Springfield notified 575 patients early this year that they were potentially exposed to infection after state inspectors, during a spot visit, found crowded and unsanitary conditions in the inpatient dialysis unit. Most of those patients received dialysis treatment in 2015 and the state Department of Public Health counted each one as a “serious reportable event.’’
Dr. Douglas Salvador, vice president of medical affairs at Baystate, said no patients are known to have contracted hepatitis B or hepatitis C, the primary concerns, as a result of the problems found in the unit.
During their January visit, health department inspectors found that the hospital did not follow proper infection control practices. Staff did not set aside dialysis machines for use only on patients with hepatitis B, and did not always thoroughly clean those machines before they were returned for use on other patients, investigators said. Dialysis is a treatment that uses a special machine to remove harmful wastes, salt, and excess fluid from the blood of patients with kidney failure.

Total number of serious preventable medical errors in acute care hospitals by year
2015 saw a large increase in the number of errors reported. Note: The significant increase in the number of errors reported from 2012 to 2013 can be attributed to the adoption of new definitions. The increase last year is largely due to problems at one hospital.

Baystate also exceeded its limit of eight dialysis patients per shift by crowding patients between stations and using portable machines, increasing the risk of contamination from blood splattering, inspectors found.
Salvador said the hospital is now isolating machines for use only on infected patients and no longer exceeds the limit on patients. He said the machines were being cleaned thoroughly, but that nurses were not always documenting their efforts.
“There are people who come in through the emergency department and need dialysis services, and the desire is to do one more and try to get them done,’’ he said. “There were a lot of good intentions.’’
A case of contamination of equipment at a second, unidentifed hospital also contributed to the overall increase.
The state Department of Public Health tracks preventable medical errors and releases the data annually to encourage hospitals and other providers to improve the quality of care. Research studies show that as many as one-third of patients nationally are harmed during their hospitalization, health officials said. Hospitals and outpatient surgery centers also are required to report these errors to patients who are impacted and their insurers.
Most categories of preventable errors fluctuate up and down from year to year. The data “reported in Massachusetts doesn’t tell us whether medical errors are increasing,’’ said Barbara Fain, executive director of the The Betsy Lehman Center, a state agency focused on improving patient safety.
Errors could be increasing because of pressure to serve sicker patients more quickly. But more reported errors could mean hospitals are getting better at detecting problems. And facilities that report more errors are not necessarily providing inferior care; they may do a better job of spotting harm and then correcting problems.
Fain also pointed out that the state data include only hospitals and surgery centers. “That leaves out many other settings where we know serious medical errors take place, like doctors’ offices and nursing homes,’’ she said. “Without more complete data it’s simply not possible to determine trends.’’
According to the health department report, surgical errors, such as leaving an instrument inside a patient, increasingly occur outside of operating rooms, in radiology, labor and delivery, and inpatient units. Falls and pressure ulcers are the two most common types of preventable incidents in most years.
Notably, 59 ambulatory surgery centers reported just four errors last year. They do not have as much experience as hospitals in developing systems to identify and track serious problems, underscoring the difficulty of drawing conclusions from the numbers.
“We’re concerned about the low level of reporting by (surgery centers) and that’s the reason for our initiatives,’’ said Fain, whose organization has developed an online tool to help providers identify and report errors.
Baystate Medical Center in Springfield notified 575 patients early this year that they were potentially exposed to infection after state inspectors, during a spot visit, found crowded and unsanitary conditions in the inpatient dialysis unit. Most of those patients received dialysis treatment in 2015 and the state Department of Public Health counted each one as a “serious reportable event.’’
Dr. Douglas Salvador, vice president of medical affairs at Baystate, said no patients are known to have contracted hepatitis B or hepatitis C, the primary concerns, as a result of the problems found in the unit.
During their January visit, health department inspectors found that the hospital did not follow proper infection control practices. Staff did not set aside dialysis machines for use only on patients with hepatitis B, and did not always thoroughly clean those machines before they were returned for use on other patients, investigators said. Dialysis is a treatment that uses a special machine to remove harmful wastes, salt, and excess fluid from the blood of patients with kidney failure.

Liz Kowalczyk can be reached at Follow her on Twitter @GlobeLizK.

Aquatic treadmill walking may increase exercise capacity after stroke

And how many stroke departments do you think have this? I'd say none except for this one. The hospital I was at gave up their pool years before.Useless because 10 or so people might be able to take advantage when there are 10 million survivors a year.
For patients in rehabilitation after a stroke, walking on an underwater treadmill produces better measures of exercise performance compared to conventional treadmill walking, reports a study in the American Journal of Physical Medicine & Rehabilitation.
"Aquatic treadmill exercise may be a useful option for early intensive aerobic exercise after subacute stroke, as it may both improve their aerobic capacity and maximize functional recovery," according to the preliminary research by Bo Ryun Kim, MD, PhD, and colleagues of Jeju National University Hospital, Korea.
Walking in Water May Have Advantages for Post-Stroke Rehab
The study included 21 patients recovering after a stroke—average time since their stroke was about two months. All patients had some walking ability, but with impaired leg movement on the side affected by the stroke.
The patients underwent two exercise tests: one on a conventional land treadmill and one on an aquatic treadmill, submerged in water up to their chests. In both tests, walking speed and slope were gradually increased until the patients felt they couldn't go any further. Measures of exercise capacity were compared between the two tests.Two key measures were higher on the aquatic treadmill test: maximal oxygen consumption (VO2max), reflecting heart and lung function during exercise; and metabolic equivalents (METs), reflecting energy use. Heart rate was not significantly different, but was significantly related to oxygen consumption on both tests.
Even though their was higher on the water treadmill, patients felt they weren't working as hard as on the land treadmill, based on a measure called rating of perceived exertion. "This improved performance may reflect the fact that the aquatic treadmill exercise involved the fluid resistance of the water environment," Dr. Kim and colleagues write.
Regaining walking ability is a major challenge after a stroke. Because it's so difficult to walk, patients may be physically inactive, further their reducing exercise capacity. This suggests that early intensive aerobic exercise training might be beneficial in the early weeks after stroke. Treadmill walking is commonly recommended, but may be difficult or impossible because of decreased muscle power.
"The fact that the aquatic treadmill efficiently provides aerobic exercise without requiring full weight bearing means that it may be highly suitable for rehabilitation after stroke," according to the authors. The buoyancy provided by water reduces musculoskeletal impact while allowing combined aerobic and resistance exercise. Exercising in water also has the psychological benefit of freedom from the fear of falling.
The preliminary study is the first to explore the benefits of aquatic treadmill exercise for stroke patients. Further research will be needed to determine whether this approach leads to lasting improvements in exercise capacity and walking ability, several months after the stroke.
If so, then approaches including underwater treadmill exercise may help to overcome the low aerobic capacity seen in stroke survivors—which can contribute to decreased social activity and poor quality of life. Dr. Kim and colleagues conclude, "Aquatic may not only improve baseline functional status and functional recovery during the subacute period, it may also enhance social participation and quality of life during the chronic period."
More information: Yong Ki Lee et al. Peak Cardiorespiratory Responses of Patients with Subacute Stroke During Land and Aquatic Treadmill Exercise, American Journal of Physical Medicine & Rehabilitation (2016). DOI: 10.1097/PHM.0000000000000603

Journal reference: Archives of Physical Medicine and Rehabilitation search and more info website

Tuesday, August 23, 2016

I blog because...

It started by being challenged by Peter Levine to write one.  Luckily I put Musings in my title, that allowed me to write about anything I wanted to rather than be constrained by sticking to stroke rehab. I write because I see the failings of the stroke world and are easily able to identify what should be done to solve for those failings.No one in charge seems to read or listen to me. I have received maybe a couple of positive reviews from therapists, nothing from any doctors or stroke association officials. I may be tilting at windmills but I know I am right and will continue my quest for worldwide domination. Worldwide domination is so much easier than trying to convince supposedly smart stroke medical people that they have no fucking clue how to solve stroke. Ah well, my grandiosity on display.  Written because of My Brain Lesion and Me - Rhiann

The Role of Caffeine in Artery Function

You can decide for yourself what you want to do about coffee and caffeine. For me there are way too many benefits, written about in these 102 posts on coffee and 47 posts on caffeine.

THC makes rats lazy, less willing to try cognitively demanding tasks: UBC study

I would think that the higher reasoning displayed by most adults could easily counteract this. But negative articles like this will continue until proof of marijuana usefulness overwhelms the naysayers by your Mom and grandmmothers positive experiences.
New research from the University of British Columbia suggests there may be some truth to the belief that marijuana use causes laziness— at least in rats.
The study, published today in the Journal of Psychiatry and Neuroscience, found that tetrahydrocannabinol (THC), the main psychoactive ingredient in marijuana, makes rats less willing to try a cognitively demanding task.
“Perhaps unsurprisingly, we found that when we gave THC to these rats, they basically became cognitively lazy,” said Mason Silveira, the study’s lead author and a PhD candidate in UBC’s department of psychology. “What’s interesting, however, is that their ability to do the difficult challenge was unaffected by THC. The rats could still do the task— they just didn’t want to.”
For the study, researchers looked at the effects of both THC and cannabidiol (CBD) on rats’ willingness to exert cognitive effort.
They trained 29 rats to perform a behavioural experiment in which the animals had to choose whether they wanted an easy or difficult challenge to earn sugary treats.
Under normal circumstances, most rats preferred the harder challenge to earn a bigger reward. But when the rats were given THC, the animals switched to the easier option, despite earning a smaller reward.
When they looked at the effect of CBD, an ingredient in marijuana that does not result in a high, researchers found the chemical did not have any effect on rats’ decision-making or attention. CBD, which is believed to be beneficial in treating pain, epilepsy and even cancer, also didn’t block the negative effects of THC.
“This was surprising, as it had been suggested that high concentrations of CBD could modulate or reduce the negative effects of THC,” said Catharine Winstanley, senior author of the study and an associate professor in UBC’s department of psychology. “Unfortunately, that did not appear to be the case.”
Given how essential willingness to exert cognitive effort is for people to achieve success, Winstanley said the findings underscore the importance of realizing the possible effect of cannabis use on impairing willingness to engage in harder tasks.
While some people view marijuana as a panacea that can cure all ailments, the findings also highlight a need for more research to determine what THC does to the human brain to alter decision-making. That could eventually allow scientists to block these effects of THC, allowing those who use medical marijuana to enjoy the possible benefits of cannabis without the less desirable cognitive effects.
At the beginning of each behavioural experiment, rats chose between two levers to signal whether they wanted an easy or hard challenge.
Choosing the easy challenge resulted in a light turning on for one second, which the rats could easily detect and respond to by poking it with their nose, receiving one sugar pellet as a reward. In the more difficult challenge, the light turned on for only 0.2 seconds, rewarding the rat with two sugar pellets if they responded with a nose poke.

Stem Cell Therapy for Traumatic Brain Injury Clinical Trial - UCSF

The University of California, San Francisco has posted information about a stem cell therapy clinical trial program for eligible individuals. I can't tell if this is a valid study at all since they don't mention measuring stem cells that survived.
A Traumatic Brain Injury (TBI) occurs when a bump, blow, or jolt to the head causes injury to the brain. Falls, sports injuries, motor vehicle accidents, and violence are common causes of TBI.

We are seeking individuals who have had Traumatic Brain Injury (TBI) to participate in current and future research studies for the treatment of TBI. We are currently seeking participants in a clinical trial of modified stem cell therapy for TBI called STEMTRA (STEM cell therapy for TRAumatic brain injury).

Interested participants will complete a questionnaire for a TBI research participant recruitment registry. The information in the registry will be used to identify potential participants for STEMTRA and future clinical research studies.

You may enroll in the participant recruitment registry for TBI research if you:

  • Are age 18 or older
  • Have suffered TBI
  • Have ongoing symptoms as a result of the TBI

Note: Other inclusion and exclusion criteria apply for each study.

The STEMTRA Study, a Phase II clinical trial, is designed to test the safety and efficacy of a modified stem cell therapy that is administered directly to the injured brain through a neurosurgical procedure. Participants will have approximately seven follow-up visits for additional examinations, questionnaires, video recordings, and brain scans over the following 12 months. (See About the Registry for additional details.)

We have developed the online eligibility questionnaire to help to see if you might be a candidate for this research study or for future research studies for TBI. The questionnaire includes detailed questions about your medical history and post-TBI symptoms and takes about 30 minutes to complete.
Eligibility Questionnaire Step 1: Overview

Information from individuals who complete this questionnaire will be placed in our Participant Recruitment Registry for TBI Research. We will use this information to begin the process of helping you to determine your potential eligibility for the STEMTRA Study and for future studies for TBI. We may also contact you to obtain additional information and to tell you more about future studies that you may qualify for.

8 Common Habits that May Cause Brain Stroke

With no research link this is totally worthless. Can't tell if the conclusions are based upon research results and interpreted correctly.
According to Dutch researchers there are at least 8 habits that have been identified as risk factors for a brain stroke, or aneurysm. These eight risk factors are the following:
• Excessive coffee consumption
• Intense physical exercise
• Blowing your nose
• Extra effort when going to the bathroom
• Sodas
• Anger and stress
These behavior increase blood pressure temporarily and allow the vein breakage into an aneurysm. To detect risk factors they performed a 3 year study on people that had suffered a stroke, performing intense research in what habits and attitudes were part of their routine before the stroke. Some of the interesting factors show that people who drank coffee had twice the risk of stroke one hours after drinking the beverage. The next high-risk habits were intense exercise, blowing your nose very hard, and having $e*u@l relations.
A stroke is an expansion of arterial walls of the brain, symptoms include vomiting, visual difficulties, loss of consciousness, and intense headache. Most of these symptoms are not noticeable until they are intense enough to make people stop their regular activities. When an aneurysm breaks it causes a brain hemorrhage.
With modern neuroimaging techniques its possible to detect aneurysms, however the causes of what produces this phenomonon are still unclear. Until now being a woman and hypertension were two risk factors most identified in clinical trials.
Around 2% of Americans, 6 million people,have brain aneurysms, most of them do not break. If people limit coffee they can reduce risk by 10%, or 4% if you begin taking laxatives. These hemorrhages cause death in about 1/3 of people who suffer an aneurysm, around 2 million people just in the U.S. and leave around 20% with chronic and permanent cognitive or motor impairment.
Most aneurysms don’t rupture, create problems, or have any symptoms. This is a double-edged sword, not feeling symptoms does not mean there is not damage occurring.
Stroke victims require intensive care and minimal stress.
Most aneurysms are treated with endovascular techniques such as coiling and stenting or a combination of both. Screening tests are run to determine the effects of the aneurysm, including cerebrospinal fluid examination, imaging, or computerized tomography. Some cognitive or motor impairment can be seen in those affected, including stiffness, paralysis, pain, or motor imbalances. Surgical clipping is a technique used for closing the aneurysm which is effective in most cases. This procedure has some risks to the brain such as blood flow damage. Once detected, most brain aneurysms can be repaired by microsurgery. This type of surgery is performed with the aid of a microscope and tiny instruments. During surgery, the aneurysm is identified and removed, whereupon it is closed wound.
If you have a first-degree relative who has been diagnosed with an aneurysm, you should undergo evaluation and exploration for aneurysms. In most cases it’s not inherited, there are cases in which more than one family member developed aneurysms.

 A lifestyle that promotes the health of your blood vessels can also provide benefits for the prevention of aneurysms:
· No smoking
· Exercise regularly
· Eat a balanced diet
· Check blood pressure.

ableX Stroke Recovery

In case you want to attempt to influence the thick skulls at your stroke hospital for rehab machines. I have no idea of the efficacy of these. Your stroke department should be able to find out and tell you if this is the best out there. But they will have no fucking clue. You once again are completely on your own.  They are in use at Boroondara, Australia in case your doctor wants to contact the hospital there. He or she won't but that will just prove the total incompetence of your stroke rehab department.

History of stroke may increase risk for late-onset Alzheimer’s disease

So, What the fuck is your doctor doing to prevent that from happening to you?
Throwing their hands up is not an acceptable answer. Screaming in their faces is an acceptable reply from you. YOU have to put the monkey on their back and never let them transfer it back to you. Tell them you know all about the Harvard Business Review article on monkey on the back tossing.

History of stroke may increase risk for late-onset Alzheimer’s disease

Patients with a history of stroke have double the risk for late-onset Alzheimer’s disease in its familial and sporadic forms, researchers reported in JAMA Neurology.
However, according to the researchers, the effect of CV risk factors on Alzheimer’s disease was mediated by stroke.
Using data from the National Institute on Aging Late-Onset Alzheimer’s Disease/National Cell Repository for Alzheimer’s Disease family study (NIA-LOAD), the researchers assessed the contribution of CV risk factors and history of stroke to late-onset Alzheimer’s disease in large families with multiple family members affected by late-onset Alzheimer’s disease. Data from the Washington Heights-Inwood Columbia Aging Project were used to replicate findings.
The primary endpoint was probable or possible late-onset Alzheimer’s disease based on the National Institute of Neurological and Communicative Disorders and Stroke and the Alzheimer’s Disease and Related Disorders Association (NINCDS-ADRDA) criteria. The CV risk factors included in the study were hypertension, type 2 diabetes and CHD.
Giuseppe Tosto, MD, PhD, from Columbia University College of Physicians and Surgeons and NewYork-Presbyterian Hospital, and colleagues calculated a genetic risk score for late-onset Alzheimer’s disease using genome-wide significant single nucleotide polymorphisms except for APOE E4.
Of the 6,553 participants (mean age, 77 years; 62% women) included in the analyses from NIA-LOAD, 3,468 were diagnosed with late-onset Alzheimer’s disease. Of the 5,972 participants (mean age, 77 years; 68% women) in the replication sample, 2,684 had late-onset Alzheimer’s disease.
In the NIA-LOAD analysis, hypertension was associated with a lower risk for late-onset Alzheimer’s disease (OR = 0.63; 95% CI, 0.55-0.72), whereas a history of stroke was associated with twice the risk for late-onset Alzheimer’s disease (OR = 2.23; 95% CI, 1.75-2.83). No associations were observed between late-onset Alzheimer’s disease and type 2 diabetes or CHD.
In the replication study, hypertension did not have an association with late-onset Alzheimer’s disease, nor did any of the other CV risk factors. However, a relationship was again found between late-onset Alzheimer’s disease and history of stroke (OR = 1.96; 95% CI, 1.56-2.46).
According to the researchers, these results highlight the “complex relationship between hypertension and [late-onset Alzheimer’s disease]” as well as the “importance of interventions targeting modifiable risk factors in [late-onset Alzheimer’s disease]. Further studies with longitudinal assessment and a larger set of variables (eg, different classes of treatments) are currently needed.” by Tracey Romero
Disclosure: Tosto reports no relevant financial disclosures. Please see the full study for a list of all other researchers’ relevant financial disclosures.

Physiatrist referral preferences for postacute stroke rehabilitation

The only physiatrist referral reporting should have been on the efficacy of the therapists and protocols used. If you don't know the factual objective basis of survivor recovery by specific therapists then you shouldn't refer them. Doctors should not be perpetuating a failing system.

Author Information

aDepartment of Rehabilitation and Regenerative Medicine, Columbia University College of Physicians and Surgeons
bDivision of Rehabilitation Medicine, Weill Cornell Medical College
cNew York-Presbyterian Hospital, New York, NY.
Correspondence: David J. Cormier, Department of Rehabilitation and Regenerative Medicine, Columbia University Medical Center, Harkness Pavilion Room HP-1-165, 180 Fort Washington Ave., New York, NY 10032 (e-mail:
Abbreviations: AAPM&R = American Academy of Physical Medicine and Rehabilitation, ADLs = activities of daily living, IRF = inpatient rehabilitation facilities, LTACH = long-term acute care hospital, MCA = middle cerebral artery, SNF = skilled nursing facilities.
The authors report no conflicts of interest.
This is an open access article distributed under the Creative Commons Attribution License 4.0, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Received February 25, 2016
Received in revised form June 13, 2016
Accepted July 3, 2016


Abstract: This study was intended to determine if there is variation among physiatrists in referral preferences for postacute rehabilitation for stroke patients based on physician demographic characteristics or geography.
A cross-sectional survey study was developed with 5 fictional case vignettes that included information about medical, social, and functional domains. Eighty-six physiatrist residents, fellows, and attendings were asked to select the most appropriate postacute rehabilitation setting and also to rank, by importance, 15 factors influencing the referral decision. Chi-square bivariate analysis was used to analyze the data.
Eighty-six surveys were collected over a 3-day period. Bivariate analysis (using chi-square) showed no statistically significant relationship between any of the demographic variables and poststroke rehabilitation preference for any of the cases. The prognosis for functional outcome and quality of postacute facility had the highest mean influence ratings (8.63 and 8.31, respectively), whereas location of postacute facility and insurance had the lowest mean influence ratings (5.74 and 5.76, respectively).
Physiatrists’ referral preferences did not vary with any identified practitioner variables or geographic region; referral preferences only varied significantly by case.
Back to Top | Article Outline

1 Introduction

Nearly 800,000 individuals experience a stroke each year in the United States, at a cost of 33.6 billion dollars.[1] Whereas some persons with stroke recover fully, many are left with substantial disability. Stroke is the leading cause of serious long-term disability in this country.[1] Given the impact on individuals with stroke and the substantial resources devoted to their care, it is important to gain a greater understanding of which poststroke interventions lead to the best outcomes. One area of controversy is the type of rehabilitation facility where persons with stroke should receive their rehabilitative care.
Poststroke rehabilitation options include inpatient rehabilitation facilities (IRFs), skilled nursing facilities (SNFs), long-term acute care hospitals (LTACHs), home therapy, and outpatient therapy. The process of assessing rehabilitation needs and selecting the most appropriate rehabilitation option for a person with acute stroke is complex and not well-studied. Depending on the institution, this determination may be made by nurses, case managers, social workers, physical therapists, occupational therapists, speech and language pathologists, and/or physicians (including physiatrists, neurologists, internists, and others). Physiatrists’ role in this process varies among hospitals, with some hospitals involving physiatry routinely, and others rarely or never. Physiatrists’ role includes the medical and functional assessment as it encompasses all of the rehabilitation needs, through a strong relationship within the interdisciplinary rehabilitation team. Physiatrists are arguably the physicians with the most specific training in stroke rehabilitation, and it is therefore important to better understand their referral preferences for these patients.
Many factors may be considered when determining the most appropriate poststroke rehabilitation option for a given patient. These factors may include the severity and nature of neurological and functional deficits, medical comorbidities, provider and facility relationships, insurance coverage, cost, geographical proximity and location of available facilities, and patient and family preference.[2,3] When referral to an IRF is being considered, the question of whether or not a patient will be able to participate in and benefit from the 3 hours of therapy that are mandated in an IRF is of particular concern.
Assessment protocols are not standardized, and there is little reassurance that patients are reliably receiving the most appropriate rehabilitation. Furthermore, there exist no standardized criteria or guidelines to assist referral teams in predicting which poststroke discharge option is optimal for each patient. To optimize patient outcomes after stroke, more information is needed about which patients benefit most from rehabilitation in each setting. Knowing who is making these referral decisions and how they are making them is an important first step towards reaching this goal.
Given the large number of individuals involved in making decisions regarding rehabilitation level of care, and the many factors that contribute to this decision, it is unsurprising that research has found variation in referral patterns. After stroke, patients are more likely to be evaluated for rehabilitation needs if they are hospitalized in a stroke unit.[4] Measures of activities of daily living (ADLs) ability after stroke are predictive of discharge home versus a rehabilitation institution, but do not distinguish between patients discharged to SNF and patients discharged to IRF.[5]
When rehabilitation consultation teams assist in making the referral decision, patient outcomes improve.[6] Ilet et al[7] further found that the likelihood of discharge to a rehabilitation unit is influenced by variation in practice among hospitals. Geographic proximity to an IRF has been shown to be a substantial predictor of the likelihood of discharge to IRF.[8] Variation in the utilization and intensity of poststroke rehabilitation services has also been demonstrated by Medicare beneficiaries’ payment analysis.[9,10]
Patients who suffer a stroke benefit from early rehabilitation.[11,12] There is also some indication in the literature that patients admitted to IRF experience better functional recovery than those admitted to SNF.[13–17] To date, studies comparing IRF to SNF outcomes in the United States have all been observational in nature, and no randomized studies have been performed. As a result, comparing IRF to SNF stroke rehabilitation outcomes is complicated by the differences between the patient populations referred for these 2 different types of care. Multiple factors known to influence outcomes after stroke (age, cognition, functional level, continence) have also been found to be different in those receiving postacute stroke rehabilitation in IRFs and those receiving this rehabilitation in SNF.[6]
We sought to examine postacute stroke rehabilitation referral preferences among physiatrists. We hypothesized that there is variation among physiatrists in referral preferences based on demographic variables and/or geographic location, leading to patients with similar backgrounds and functional limitations being referred to different types of rehabilitation. Given that different rehabilitation options have different outcomes, this variation in referral preferences may lead to suboptimal rehabilitation outcomes for some stroke patients.[5]

More at link.

Assessment of reporting quality in randomised controlled trials of acupuncture for post-stroke rehabilitation using the CONSORT statement and STRICTA guidelines

There can be no quality reporting of acupuncture studies since energy meridians have never been proven. The placebo effect is strong in this one and grifting must be good.
  1. Lihong Lu1
+ Author Affiliations
  1. 1Guangzhou University of Chinese Medicine, Guangzhou, China
  2. 2Department of Acupuncture, First Affiliated Hospital, Guangzhou University of Chinese Medicine, Guangzhou, China
  3. 3Department of Acupuncture, Guangzhou Hospital of Traditional Chinese Medicine, Guangzhou, China
  4. 4Key Unit of Methodology in Clinical Research, Guangdong Provincial Hospital of Chinese Medicine, Guangzhou, China
  1. Correspondence to Professor Guohua Lin, Department of Acupuncture, First Affiliated Hospital, Guangzhou University of Chinese Medicine, Guangzhou 510405, China;
  • Accepted 23 July 2016
  • Published Online First 17 August 2016


Objectives To evaluate the completeness of reporting of randomised controlled trials (RCTs) of acupuncture for post-stroke rehabilitation in order to provide information to facilitate transparent and more complete reporting of acupuncture RCTs in this field.
Methods Multiple databases were searched from their inception through September 2015. Quality of reporting for included papers was assessed against a subset of criteria adapted from the Consolidated Standards for Reporting Trials (CONSORT) 2010 statement and the Standards for Reporting Interventions in Controlled Trials of Acupuncture (STRICTA) guidelines. Each item was scored 1 if it was reported, or 0 if it was not clearly stated. Descriptive statistical analysis was performed. Cohen's κ-statistics were calculated to assess agreement between the two reviewers.
Results A total of 87 RCTs were included in the full text. Based on CONSORT, good reporting was evident for items ‘‘Randomised’ in the title or abstract’, ‘Participants’, ‘Statistical methods’, ‘Recruitment’, ‘Baseline data’, and ‘Outcomes and estimation’, with positive rates >80%. However, the quality of reporting for the items ‘Trial design’, ‘Outcomes’, ‘Sample size’, ‘Allocation concealment’, ‘Implementation’, ‘Blinding’, ‘Flow chart’, ‘Intent-to-treat analysis’, and ‘Ancillary analyses’ was very poor with positive rates <10%. Based on STRICTA, the items ‘Number of needle insertions per subject per session’, ‘Responses sought’, and ‘Needle type’ had poor reporting with positive rates <50%. Substantial agreement was observed for most items and good agreement was observed for some items.
Conclusions The reporting quality of RCTs in acupuncture for post-stroke rehabilitation is unsatisfactory and needs improvement.