“Unless someone like YOU cares a whole awful lot, Nothing is going to get better. It's not.” Dr. Seuss, The Lorax

It's all up to YOU, if YOU think the current stroke rehabilitation and protocols are just fine then you are absolved of all responsibility for trying to make it better. If not, then you should be screaming in every stroke medical persons' face you know that, 'Everything in stroke is a fucking failure.' 'What are you doing to change that?'

http://cdn2.hellogiggles.com/wp-content/uploads/2014/09/09/lorax1.jpg

Effect of Hyperacute Administration (Within 6 Hours) of Transdermal Glyceryl Trinitrate, a Nitric Oxide Donor, on Outcome After Stroke: Subgroup Analysis of the Efficacy of Nitric Oxide in Stroke (ENOS) Trial

Well, if this is effective, what about having stroke survivors breath nitric oxide and eat nitrate rich foods that convert to nitric oxide?  Damn, these are fucking simple questions that should have popped into any stroke medical persons mind and suggested changes to our non-existent stroke strategy. You want to train your doctor on this? I have 56 posts on nitric oxide. Go for the training. It's all up to YOU because your doctors are going to do nothing with this.
http://www.ncbi.nlm.nih.gov/pubmed/26463698

Woodhouse L¹, Scutt P¹, Krishnan K¹, Berge E¹, Gommans J¹, Ntaios G¹, Wardlaw J¹, Sprigg N¹, Bath PM²; ENOS Investigators.

Author information

Abstract

BACKGROUND AND PURPOSE:

Nitric oxide donors are candidate treatments for acute stroke, potentially through hemodynamic, reperfusion, and neuroprotectant effects, especially if given early. Although the large Efficacy of Nitric Oxide in Stroke (ENOS) trial of transdermal glyceryl trinitrate (GTN) was neutral, a prespecified subgroup suggested that GTN improved functional outcome if administered early after stroke onset.

METHODS:

Prospective analysis of subgroup of patients randomized into the ENOS trial within 6 hours of stroke onset. Safety and efficacy of GTN versus no GTN were assessed using data on early and late outcomes.

RESULTS:

Two hundred seventy-three patients were randomized within 6 hours of ictus: mean (SD) age, 69.9 (12.7) years; men, 154 (56.4%); ischemic stroke, 208 (76.2%); Scandinavian Stroke Scale, 32.1 (11.9); and total anterior circulation syndrome, 86 (31.5%). When compared with no GTN, the first dose of GTN lowered blood pressure by 9.4/3.3 mm Hg (P<0.01, P=0.064) and shifted the modified Rankin Scale to a better outcome by day 90, adjusted common odds ratio, 0.51 (95% confidence interval, 0.32-0.80). Significant beneficial effects were also seen with GTN for disability (Barthel Index), quality of life (EuroQol-Visual Analogue Scale), cognition (telephone Mini-Mental State Examination), and mood (Zung Depression Scale). GTN was safe to administer with less serious adverse events by day 90 (GTN 18.8% versus no GTN 34.1%) and death (hazard ratio, 0.44; 95% confidence interval, 0.20-0.99; P=0.047).

CONCLUSIONS:

In a subgroup analysis of the large ENOS trial, transdermal GTN was safe to administer and associated with improved functional outcome and fewer deaths when administered within 6 hours of stroke onset.

CLINICAL TRIAL REGISTRATION:

URL: http://www.clinicaltrials.gov. Unique identifier: NCT00989716.

Stroke Rounds: Post-Acute Peptide Tx Reduces Disability

How many decades is this going to take before it becomes a standard stroke protocol? After further good test results? Unless YOU start screaming at your doctors and hospital this won't occur for 50 years. It is all up to YOU, since we have no great stroke association taking care of these simple tasks. Any clinical study using the Rankin scale to measure results is deceiving themselves that it is a valid measurement tool. There is nothing objective about it, except 6 - dead. This is something a great stroke association would be doing, training clinical researchers in how to properly run research trials.
http://www.medpagetoday.com/Cardiology/Strokes/54821?xid=nl_mpt_cardiodaily_2015-11-20&eun=gd3r
Injections of the product sold as Cerebrolysin in Russia, China, and surrounding countries had a "large" effect size on the Action Research Arm Test (ARAT) score on day 90 compared with placebo (Mann-Whitney estimator 0.71, P<0.0001).

"The multivariate effect size on global status, as assessed using 12 different outcome scales, indicated a small-to-medium superiority of Cerebrolysin, (Mann-Whitney estimator 0.62; 95% CI 0.58-0.65; P<0.0001)," Dafin F. Muresanu, PhD, of "Iuliu Hatieganu" University of Medicine and Pharmacy in Napoca, Romania, and colleagues found.
The proportion of patients with minimal disability at 90 days, marked by a modified Rankin Scale (mRS) score of 0 to 1, was 42.3% with the injections compared with 14.9% on placebo, the researchers reported online in Stroke.
The intervention likewise up-shifted the proportion of patients with a "good" functional outcome marked by mRS scores of 2 or less.
Cerebrolysin is a mixture of low molecular weight neuropeptides and free amino acids derived from pig brain tissue through a standardized manufacturing process.
"No one knows exactly what's in there, nevertheless it has a very strong track record in animal models," commented Costantino Iadecola, MD, director of Cornell's Brain and Mind Research Institute in New York City.

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The findings were promising as there's little other than rehabilitation to offer patients in the post-acute phase, he said. "Many of the drugs we have were originally developed from biological material and we had to use molecular biology to develop recombinant forms and control adverse effects."
But he warned against trying to import the substance, as one Alzheimer's group has noted can be done.
"Before the I's are dotted and the T's are crossed, don't rush into treatment," Iadecola cautioned, noting that the small studies done so far are not enough to establish safety in terms of antibody development and even possibly prion diseases, which could take years to show up.
The CARS trial randomized 208 moderate-to-severe stroke patients to double-blind treatment with Cerebrolysin (once-daily 30 mL injections) or saline placebo for 21 days, starting 24 to 72 hours after onset, along with a standardized rehabilitation program for all patients.
Baseline stroke severity, disability, and other characteristics were similar between groups.

"Cerebrolysin was safe and well tolerated," the researchers noted, pointing to a 3.8% rate of premature discontinuation.
"This study was planned as an exploratory phase II trial," Muresanu's group wrote. "This design limits the degree of evidence obtained; thus, the results should be confirmed in a large-scale phase III trial. In addition, the generalizability of our results to other regions and stroke populations should be evaluated in future research."

The study was funded by EVER Neuro Pharma.
Muresanu disclosed relationships with EVER Neuro Pharma.
Iadecola disclosed having no relevant relationships with industry.

• Primary Source

  Stroke

  Source Reference: Muresanu DF, et al "Cerebrolysin and recovery after stroke (CARS): A randomized, placebo-controlled, double-blind, multicenter trial" Stroke 2016; DOI: 10.1161/STROKEAHA.115.009416.

A New Way to Diagnose Brain Damage from Concussions, Strokes, and Dementia

I'm betting 50 years before this gets to your hospital unless YOU start agitating to your hospital president. Bypass the stroke department head because that person  likely has not pushed anything new to the stroke department since getting installed. I'm hoping I get lots of nasty comments from department heads. You'll have to tell whomever is scanning you that you had previous damage from a stroke so they don't misinterpret the scan.

A New Way to Diagnose Brain Damage from Concussions, Strokes, and Dementia

New optical diagnostic technology developed at Tufts University School of Engineering promises new ways to identify and monitor brain damage resulting from traumatic injury, stroke or vascular dementia—in real time and without invasive procedures.Coherent hemodynamics spectroscopy (CHS), developed and published by Tufts Professor of Biomedical Engineering Sergio Fantini, measures blood flow, blood volume, and oxygen consumption in the brain. It uses non-invasive near infrared (NIR) light technology to scan brain tissue, and then applies mathematical algorithms to interpret that information. "CHS is based on measurements of brain hemodynamics that are interpreted according to unique algorithms that generate measures of cerebral blood flow, blood volume and oxygen consumption," says Fantini. "This technique can be used not only to assess brain diseases but also to study the blood flow and how it is regulated in the healthy brain. "Tufts has licensed CHS on a non-exclusive basis to ISS, a Champaign, Ill.-based company that specializes in technology to measure hemoglobin concentration and oxygenation in brain and muscle tissue. "Potentially the market for CHS is large as it encompasses several applications from the monitoring of cerebrovascular disorders to assessing neurological disorders," says Beniamino Barbieri, president of ISS. "It reminds me of the introduction of ultrasound technology at beginning of the seventies; nobody back then knew how to utilize the new technology and of course, nowadays, its applications are ubiquitous in any medical center."

How It Works

CHS uses laser diodes which emit NIR light that is delivered to the scalp by fiber optics. Light waves are absorbed by the blood vessels in the brain. Remaining light is reflected back to sensors, resulting in optical signals that oscillate with time as a result of the heartbeat, respiration, or other sources of variations in the blood pressure.

By analyzing the light signals with algorithms developed for this purpose, Fantini's model is able to evaluate blood flow and the way the brain regulates it--which is one marker for brain health. CHS technology has been tested among patients undergoing hemodialysis at Tufts Medical Center. Published research reported a lower cerebral blood flow in dialysis patients compared with healthy patients. "Non-invasive ways to measure local changes in cerebral blood flow, particularly during periods of stress such as hemodialysis, surgeries, and in the setting of stroke, could have major implications for maintaining healthy brain function," says Daniel Weiner, M.D., a nephrologist at Tufts Medical Center (Tufts MC) and associate professor of medicine at Tufts University School of Medicine (TUSM), who is a member of the research team. Josh Kornbluth, M.D., a neurologist at Tufts MC and associate professor of medicine at TUSM, is also working with Fantini to explore CHS's potential to assess the cerebrovascular state of patients who suffer traumatic brain injury or stroke. They hope to test CHS further among neurological critical care patients. "Having data about local cerebral blood flow and whether it is properly regulated can allow us to more accurately develop individualized therapy and interventions instead of choosing a 'one size fits all' approach to traumatic brain injury, stroke, or subarachnoid hemorrhage," Kornbluth says. Located on Tufts' Medford/Somerville campus, Tufts University School of Engineering offers a rigorous engineering education in a unique environment that blends the intellectual and technological resources of a world-class research university with the strengths of a top-ranked liberal arts college. Close partnerships with Tufts' excellent undergraduate, graduate and professional schools, coupled with a long tradition of collaboration, provide a strong platform for interdisciplinary education and scholarship. The School of Engineering’s mission  is to educate engineers committed to the innovative and ethical application of science and technology in addressing the most pressing societal needs, to develop and nurture twenty-first century leadership qualities in its students, faculty, and alumni, and to create and disseminate transformational new knowledge and technologies that further the well-being and sustainability of society in such cross-cutting areas as human health, environmental sustainability, alternative energy, and the human-technology interface.  

New optical diagnostic technology developed at Tufts University School of Engineering promises new ways to identify and monitor brain damage resulting from traumatic injury, stroke or vascular dementia—in real time and without invasive procedures.
Coherent hemodynamics spectroscopy (CHS), developed and published by Tufts Professor of Biomedical Engineering Sergio Fantini, measures blood flow, blood volume, and oxygen consumption in the brain. It uses non-invasive near infrared (NIR) light technology to scan brain tissue, and then applies mathematical algorithms to interpret that information.
"CHS is based on measurements of brain hemodynamics that are interpreted according to unique algorithms that generate measures of cerebral blood flow, blood volume and oxygen consumption," says Fantini. "This technique can be used not only to assess brain diseases but also to study the blood flow and how it is regulated in the healthy brain."
Tufts has licensed CHS on a non-exclusive basis to ISS, a Champaign, Ill.-based company that specializes in technology to measure hemoglobin concentration and oxygenation in brain and muscle tissue.
"Potentially the market for CHS is large as it encompasses several applications from the monitoring of cerebrovascular disorders to assessing neurological disorders," says Beniamino Barbieri, president of ISS. "It reminds me of the introduction of ultrasound technology at beginning of the seventies; nobody back then knew how to utilize the new technology and of course, nowadays, its applications are ubiquitous in any medical center."
How It Works
CHS uses laser diodes which emit NIR light that is delivered to the scalp by fiber optics. Light waves are absorbed by the blood vessels in the brain. Remaining light is reflected back to sensors, resulting in optical signals that oscillate with time as a result of the heartbeat, respiration, or other sources of variations in the blood pressure.
By analyzing the light signals with algorithms developed for this purpose, Fantini's model is able to evaluate blood flow and the way the brain regulates it--which is one marker for brain health.
CHS technology has been tested among patients undergoing hemodialysis at Tufts Medical Center. Published research reported a lower cerebral blood flow in dialysis patients compared with healthy patients. "Non-invasive ways to measure local changes in cerebral blood flow, particularly during periods of stress such as hemodialysis, surgeries, and in the setting of stroke, could have major implications for maintaining healthy brain function," says Daniel Weiner, M.D., a nephrologist at Tufts Medical Center (Tufts MC) and associate professor of medicine at Tufts University School of Medicine (TUSM), who is a member of the research team.
Josh Kornbluth, M.D., a neurologist at Tufts MC and associate professor of medicine at TUSM, is also working with Fantini to explore CHS's potential to assess the cerebrovascular state of patients who suffer traumatic brain injury or stroke. They hope to test CHS further among neurological critical care patients.
"Having data about local cerebral blood flow and whether it is properly regulated can allow us to more accurately develop individualized therapy and interventions instead of choosing a 'one size fits all' approach to traumatic brain injury, stroke, or subarachnoid hemorrhage," Kornbluth says.
Located on Tufts' Medford/Somerville campus, Tufts University School of Engineering offers a rigorous engineering education in a unique environment that blends the intellectual and technological resources of a world-class research university with the strengths of a top-ranked liberal arts college. Close partnerships with Tufts' excellent undergraduate, graduate and professional schools, coupled with a long tradition of collaboration, provide a strong platform for interdisciplinary education and scholarship. The School of Engineering’s mission  is to educate engineers committed to the innovative and ethical application of science and technology in addressing the most pressing societal needs, to develop and nurture twenty-first century leadership qualities in its students, faculty, and alumni, and to create and disseminate transformational new knowledge and technologies that further the well-being and sustainability of society in such cross-cutting areas as human health, environmental sustainability, alternative energy, and the human-technology interface
- See more at: http://now.tufts.edu/news-releases/new-way-diagnose-brain-damage-concussions-strokes-and-dementia#sthash.xVrDTpyu.dpuf

Sound Mind, Strong Heart: Same Protein Sustains Both

So what protocol is your doctor giving you to make sure your BDNF levels are adequate? Does your doctor know anything about this? This is still only in rodents so 50 years before it makes it to humans unless YOU raise some hell to get it researched.
http://www.hopkinsmedicine.org/news/media/releases/sound_mind_strong_heart_same_protein_sustains_both

A Roman philosopher was the first to note the relationship between a sound mind and a sound body. Now the findings of a new Johns Hopkins study reveal a possible biochemical explanation behind this ancient observation.

The research, published ahead of print Jan. 12 in the Proceedings of the National Academy of Sciences, reveals that a protein already known to act as a natural antidepressant, enhance learning and memory, power nerve cell growth, and nourish blood vessels is also a central player in maintaining heart muscle vitality.

The team’s experiments, conducted in mice and lab-grown heart cells, show this multi-tasking protein, a nerve-growth factor called BDNF (brain-derived neurotrophic factor), helps sustain the ability of heart muscle cells to contract and relax properly. The results reveal that either BDNF deficiency or cell insensitivity to BDNF’s presence can precipitate heart muscle dysfunction, particularly under conditions of chronic or repeated physical stress on the heart, such as endurance training or high blood pressure. Specifically, the researchers tracked BDNF’s role in a cascade of molecular signaling events in heart cells, the disruption of which led to heart muscle failure.

If confirmed in humans, the research team says, the findings could pave the way to new treatments for certain forms of heart failure, a disorder that affects nearly 6 million Americans and more than 23 million people worldwide.

In addition, because of BDNF’s well-known antidepressant effects and its role as a booster of nerve cell health, the research teams says the results suggest a possible biochemical link between depression and heart disease, two disorders that tend to occur in concert but whose relationship remains poorly understood.

“Our results are not only a vivid reminder of the astounding complexity of the heart’s chemistry and physiology, but also a striking example of the ability of a single protein to act on multiple fronts and affect many organs and functions,” says lead investigator Ning Feng, M.D., Ph.D., a cardiology fellow at the Johns Hopkins University School of Medicine.

The findings also can help clarify the biological means behind recent – and unexplained –observations that heart failure patients whose cardiac function worsens during physical exertion have low levels of BDNF in the blood.

“Our observation that BDNF directly controls the ability of heart muscle cells to ‘beat’ properly offers one possible explanation behind the declining cardiac function seen in people with heart failure, especially during exercise,” says senior author Nazareno Paolocci, M.D., Ph.D., assistant professor of medicine at the Johns Hopkins University School of Medicine.

In an initial set of experiments, the scientists isolated cardiac cells from rodents with either normal or failing hearts in a lab dish and exposed the cells to BDNF. The normal heart cells responded by contracting and relaxing vigorously in the presence of BDNF, a phenomenon marked by peaks of contraction-triggering calcium flow into the cells. However, cells obtained from failing hearts, even when awash in BDNF, responded weakly or not at all. To determine why, the team homed in on BDNF’s receptor, a molecule called TrkB, located on the surface of cells and responsible for receiving BDNF’s chemical signals and transmitting them inside the cell. Compared with cardiac cells from mice with normal hearts, the failing heart cells had a slightly different version of the TrkB receptor, one that produces less of a catalyst protein responsible for triggering critical signaling inside the cardiac cell. This slightly sub-performing version of the receptor was less responsive to BDNF, rendering the heart cell less sensitive to it. While this TrkB variant is fairly common and does not necessarily portend disease, it may render the heart cells of those who carry the altered version less capable of using BDNF, the researchers say. Mice engineered to lack TrkB receptors in their heart cells developed impaired cardiac function. Their hearts contracted poorly, pumped blood less efficiently and took longer to relax after each beat.

“Taken together, these findings show that any abnormality in the way BDNF communicates with its receptor appears to unlock a cascade of chemical glitches that eventually leads to poor cardiac function,” Feng says.

The investigators say that disruptions in proper BDNF-TrkB signaling can even explain what drives chemotherapy-induced heart failure, a serious and well-established side effect of certain cancer treatments. Such treatments include chemicals that block multiple growth-factor receptors, TrkB among them, to halt tumor growth. And while this approach is critical to stave off cancer progression, it can also inadvertently lead to heart failure by interfering with the ability of cardiac cells to respond to the BDNF circulating in the body.

Another important finding, the researchers say, is that mice with missing BDNF receptors remained sensitive to adrenaline, the neurotransmitter released during fight-or-flight situations to infuse the heart with extra energy needed for peak cardiac performance during bouts of intense physical or emotional activity. The finding, the scientists say, means that BDNF affects cardiac function independently and separately from adrenaline by providing continuous, low-level fuel for heart contraction under normal conditions or prolonged periods of slightly elevated cardiac output, such as endurance training.

“Just like a constant low flame can keep a pot on slow simmer, constant levels of BDNF seem to maintain heart muscle vitality,” Paolocci says.  

The researchers point out that low levels of BDNF by themselves may not be enough to cause immediate heart disease, but chronic BDNF deficiency or insensitivity, compounded by additional physiologic or pathologic stressors, is a main culprit in fueling the disease.

“In the absence of chronic stressors, such as hypertension or an elevated workload of the heart muscle, BDNF deficiency may not cause full-blown disease, but it could be the proverbial straw that leads to a ‘broken heart,’” Paolocci says.

The research was funded in part by the American Heart Association under grant number GRNT17070027 and by the National Institutes of Health under grant number T32HL-0227, with additional funding support from the Magic That Matters Fund of the Division of Cardiology at Johns Hopkins.

 

Effects of a Mirror-Induced Visual Illusion on a Reaching Task in Stroke Patients Implications for Mirror Therapy Training

Mirror training has been considered useful since at least 1999.
Rehabilitation of hemiparesis after stroke with a mirror
Altschuler EL, Wisdom SB, Stone L, Foster C, Galasko D, Llewellyn DME, Ramachandran V
The Lancet - Vol. 353, Issue 9169, 12 June 1999, Pages 2035-2036
15 f*cking years later and we still do not have a protocol. Does anyone in stroke do ANYTHING AT ALL?
 Who will create a defined protocol for it? Obviously not the ASA, NSA or WSO. So YOU are going to have to tackle the dangerous task  of creating your own protocol of how to look at your affected side in the mirror. Be careful of breaking that mirror.
http://nnr.sagepub.com/content/28/7/652?etoc

1. Ruud W. Selles, PhD1
2. Marian E. Michielsen, PhD1,†
3. Johannes B. J. Bussmann, PhD1
4. Henk J. Stam, MD, PhD1
5. Henri L. Hurkmans, PhD1
6. Iris Heijnen, MSc2
7. Danielle de Groot, MSc3
8. Gerard M. Ribbers, MD, PhD1,4

1. ¹Erasmus MC- University Medical Center, Rotterdam, Netherlands
2. ²Rehabilitation Centre Blixembosch, Libra Zorggroep, Eindhoven, Netherlands
3. ³Rehabilitation Centre Leijpark, Libra Zorggroep, Tilburg, Netherlands
4. ⁴Rijndam Rehabilitation Centre, Rotterdam, Netherlands
5. ^†Deceased

1. Ruud W. Selles, Department of Rehabilitation Medicine and Physical Therapy, Erasmus MC- University Medical Center, Room h.018, PO Box 2040, 3000 CE, Rotterdam, Netherlands. Email: r.selles@erasmusmc.nl

Abstract

Background. Although most mirror therapy studies have shown improved motor performance in stroke patients, the optimal mirror training protocol still remains unclear. Objective. To study the relative contribution of a mirror in training a reaching task and of unilateral and bimanual training with a mirror. Methods. A total of 93 stroke patients at least 6 months poststroke were instructed to perform a reaching task as fast and as fluently as possible. They performed 70 practice trials after being randomly allocated to 1 of 5 experimental groups: training with (1) the paretic arm with direct view (Paretic-No Mirror), (2) the nonparetic arm with direct view (Nonparetic-No Mirror), (3) the nonparetic arm with mirror reflection (Nonparetic Mirror), (4) both sides and with a nontransparent screen preventing visual control of paretic side (Bilateral-Screen), and (5) both sides with mirror reflection of the nonparetic arm (Bilateral-Mirror). As baseline and follow-up, patients performed 6 trials using only their paretic side. Primary outcome measure was the movement time. Results. We found the largest intervention effect in the Paretic-No Mirror condition. However, the Nonparetic-Mirror condition was not significantly different from the Paretic-No Mirror condition, while the Unaffected-No Mirror condition had significantly less improvement than the Paretic-No Mirror condition. In addition, movement time improved significantly less in the bimanual conditions and there was no difference between both bimanual conditions or between both mirror conditions. Conclusion. The present study confirms that using a mirror reflection can facilitate motor learning. In this task, bimanual movement using mirror training was less effective than unilateral training.

What Would Dean Do? - As head of a stroke hospital dept.

First, you have to know how bad your department is. Nothing here would require the stroke head to be a doctor.

Statistics will be kept on everything, 30 day deaths, 5 day deaths, tPA efficacy, time of tPA delivery., Correct and incorrect diagnosis in the ER of stroke vs. bad balance vs. bleeder and clot based.

This will all be compared to other hospitals and a strategic plan will be created for making each goal a perfect response(100% recovery, no 30day deaths, etc.) You may not know how to initially reach the goals but there will be no slacking off in my hospital. I expect an innovative idea from every person in the dept. on a monthly basis. This person will know every single stroke hospital and dept. head in the US. All local researchers will have office facilities and help with grants/equipment.

Actual size of each stroke dead area and penumbra area will be measured.
Stroke protocols will be created for each deficit AND each dead and damaged area.
An intern will be assigned to compile  new stroke research on a daily basis. That will be required reading and translation by all neurologists, PMR doctors, ER doctors and therapists into stroke protocols within a week.
All stroke deaths will be autopsied and dead and damaged areas compared to the initial measurements. Stroke will not be allowed as cause of death. Specific damage will be written up as to why that damage caused the death.
There will be no negativity around the patients - nocebo effect.

Man, am I arrogant.  But what is YOUR hospital doing to improve stroke rehab and recovery?  ANYTHING AT ALL? Ask for a public acknowledgement of the problems and the goals. Get With the Guidelines and Joint Commission certification are not anywhere close enough to improve stroke results. We can't wait that long. Many people will die unless YOU the public takes charge.

Let the flame wars begin, I look forward to medical apologists and their reasons for not being able to accomplish this.