Five hospitals land on national honor roll - Michigan hospitals

I really don't see this as very important. It is not Get With the Results. Get With the Guidelines is only doing processes that may or may not  result in better outcomes.
A good manager would never let you set goals on processes/guidelines. Your manager would always ask what the results were.  I would get fired if I tried to pass this off as my goals.
You can check out the guidelines here.
http://www.grbj.com/articles/80444-five-hospitals-land-on-national-honor-roll
The 2013-2014 awards acknowledge the commitment and effort hospitals have taken to improve their procedures and outcomes for cardiac and stroke patients. The five West Michigan-area organizations acknowledged for their efforts include: Bronson Methodist Hospital, Kalamazoo; Borgess Medical Center, Kalamazoo; Mercy Health Saint Mary’s Hospital, Grand Rapids; Metro Health Hospital, Wyoming; and Spectrum Health Grand Rapids, Grand Rapids.

More at link.

Botox for depression

This would be for facial muscles putting a smile on your face. I wouldn't ask your doctor giving you botox for spasticity to inject your facial muscles. That is not their area of expertise. And the forced grin looks hideous.
Psychologists call it embodied cognition.

Treatment of depression with onabotulinumtoxinA

Eric Finzi

,

Norman E. Rosenthal

Received: August 27, 2013; Received in revised form: November 13, 2013; Accepted: November 20, 2013; Published Online: December 16, 2013

DOI: http://dx.doi.org/10.1016/j.jpsychires.2013.11.006

• Abstract
• Full Text
• Images
• References
• Supplemental Materials

Abstract

Converging lines of evidence suggest a role for facial expressions in the pathophysiology and treatment of mood disorders.
To determine the antidepressant effect of onabotulinumtoxinA (OBA) treatment of corrugator and procerus muscles in people with major depressive disorder, we conducted a double blind, randomized, placebo-controlled trial. In an outpatient clinical research center, eighty-five subjects with DSM-IV major depression were randomized to receive either OBA (29 units for females and 40 units for males) or saline injections into corrugator and procerus frown muscles (74 subjects were entered into the analysis). Subjects were rated at screening, and 3 and 6 weeks after OBA treatment. The primary outcome measure was the response rate, as defined by ≥ 50% decrease in score on the Montgomery–Asberg Depression Rating Scale (MADRS). Response rates at 6 weeks from the date of injection were 52% and 15% in the OBA and placebo groups, respectively (Chi-Square (1) = 11.2, p < 0.001, Fisher p < 0.001). The secondary outcome measure of remission rate (MADRS score of 10 or less) was 27% with OBA and 7% with placebo (Chi-square (1) = 5.1, p < 0.02, Fisher p < 0.03). Six weeks after a single treatment, MADRS scores of subjects were reduced on average by 47% in those given OBA, and by 21% in those given placebo (Mann–Whitney U, p < 0.0005).
In conclusion, a single treatment with OBA to the corrugator and procerus muscles appears to induce a significant and sustained antidepressant effect in patients with major depression.

 

Who made it through to the finals of Qualcomm Tricorder X Prize?

Your hospital and ambulance crews should be following this very very closely. This could solve the current inability to objectively diagnose a stroke without expensive equipment and a neurologist on hand. A neurologist job-killer?
http://medcitynews.com/2014/08/who-made-it-through-to-the-finals-of-qualcomm-tricorder-x-prize/
Required Core Health Conditions (13): Anemia, Atrial Fibrillation (AFib), Chronic Obstructive Pulmonary Disease (COPD), Diabetes, Hepatitis A, Leukocytosis, Pneumonia, Otitis Media, Sleep Apnea, Stroke, Tuberculosis, Urinary Tract Infection, Absence of condition.

Study Questions Long-held Depression Belief

Is your doctor up on this latest research? For all the crap I went through I don't believe I've ever been depressed a day in my life.
http://www.biosciencetechnology.com/news/2014/08/study-questions-long-held-depression-belief?

The efficacy of traditional Thai massage in decreasing spasticity in elderly stroke patients

The fact that this doesn't work would be for the same reason that stretching doesn't work as explained by Peter Levine here, here and here. Any improvements would probably be due to spontaneous recovery anyway.

http://www.dovepress.com/the-efficacy-of-traditional-thai-massage-in-decreasing-spasticity-in-e-peer-reviewed-article-CIA

Authors Thanakiatpinyo T, Suwannatrai S, Suwannatrai U, Khumkaew P, Wiwattamongkol D, Vannabhum M, Pianmanakit S, Kuptniratsaikul V
Published Date August 2014 Volume 2014:9 Pages 1311—1319
DOI http://dx.doi.org/10.2147/CIA.S66416
Received 22 April 2014, Accepted 4 June 2014, Published 11 August 2014

Thanitta Thanakiatpinyo,¹ Supakij Suwannatrai,² Ueamphon Suwannatrai,² Phanitanong Khumkaew,² Dokmai Wiwattamongkol,² Manmas Vannabhum,² Somluck Pianmanakit,¹ Vilai Kuptniratsaikul<sup>1

1</sup>Department of Rehabilitation Medicine, ²Center of Applied Thai Traditional Medicine, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok, Thailand

Purpose: To study the efficacy of traditional Thai massage (TTM) versus conventional physical therapy (PT) programs in treating muscle spasticity, functional ability, anxiety, depression, and quality of life (QoL) in Thai stroke patients.
Methods: This randomized controlled trial with a blinded assessor was carried out at the Department of Rehabilitation Medicine, Siriraj Hospital (Bangkok, Thailand). The study included 50 stroke (onset ≥3 months) outpatients experiencing spasticity at the elbow or knee muscles at a grade of ≥1+ on the modified Ashworth Scale who were ≥50 years old and able to communicate. The subjects were randomly allocated to the treatment group receiving TTM (24 subjects) or the control group receiving the PT program (26 subjects). Both groups received treatment (either TTM or PT) twice a week for 6 weeks. Spasticity grade, functional ability, anxiety, depression, and QoL were measured at Week 0 and Week 6.
Results: At Week 6, the percentage of patients whose modified Ashworth Scale score had decreased by at least one grade was not statistically significant between the two groups. Both TTM and PT groups experienced a significant increase in functional ability and QoL, but no difference was found between the groups. Anxiety and depression scores showed a decreasing trend in the TTM group.
Conclusion: This preliminary report showed no evidence that TTM differed from the PT program in decreasing spasticity. However, both interventions may relieve spasticity, increase functional ability, and improve QoL after 6 weeks. Only TTM can decrease anxiety and depression scores. Further studies with adequate sample size are necessary.

Trivia

I switched from playing on Wed. nights to Tues. nights because friends are on Tues., acquaintances were on Wed. The DJ on Wed. mangled pronouncing the question. On Tues. it is on a screen. Last night we lost most of our points in rounds 1 and 2 because we got the last question of the round wrong on double down or dare. We did awful this week. The best part of this is the consumption of alcohol on the high bar stools. It requires lots of balance to make my way to the rest room. I'm probably using 110% of my brain capacity just to stay upright and functional. Use it or lose it.
Don't follow my ideas.

Lack of naturally occuring protein linked to dementia

Don't know what good this will do you since I'm sure your doctor has no way of determining this and nothing to solve it.
http://www.alphagalileo.org/ViewItem.aspx?ItemId=144759&CultureCode=en
Scientists at the University of Warwick have provided the first evidence that the lack of a naturally occurring protein is linked to early signs of dementia.
Published in Nature Communications, the research found that the absence of the protein MK2/3 promotes structural and physiological changes to cells in the nervous system. These changes were shown to have a significant correlation with early signs of dementia, including restricted learning and memory formation capabilities.
An absence of MK2/3, in spite of the brain cells (neurons) having significant structural abnormalities, did not prevent memories being formed, but did prevent these memories from being altered.
The results have led the researchers to call for greater attention to be paid to studying MK2/3.
Lead researcher and author Dr Sonia Corrêa says that “Understanding how the brain functions from the sub-cellular to systems level is vital if we are to be able to develop ways to counteract changes that occur with ageing.
“By demonstrating for the first time that the MK2/3 protein, which is essential for neuron communication, is required to fine-tune memory formation this study provides new insight into how molecular mechanisms regulate cognition”.
Neurons can adapt memories and make them more relevant to current situations by changing the way they communicate with other cells.
Information in the brain is transferred between neurons at synapses using chemicals (neurotransmitters) released from one (presynaptic) neuron which then act on receptors in the next (postsynaptic) neuron in the chain.
MK2/3 regulates the shape of spines in properly functioning postsynaptic neurons. Postsynaptic neurons with MK2/3 feature wider, shorter spines (Fig.1) than those without (Fig2) - see attached diagram and photo.
The researchers found that change, caused by MK2/3’s absence, in the spine’s shape restricts the ability of neurons to communicate with each other, leading to alterations in the ability to acquire new memories.
“Deterioration of brain function commonly occurs as we get older but, as result of dementia or other neurodegenerative diseases, it can occur earlier in people’s lives”, says Dr Corrêa. “For those who develop the early signs of dementia it becomes more difficult for them to adapt to changes in their life, including performing routine tasks.
“For example, washing the dishes; if you have washed them by hand your whole life and then buy a dishwasher it can be difficult for those people who are older or have dementia to acquire the new memories necessary to learn how to use the machine and mentally replace the old method of washing dishes with the new. The change in shape of the postsynaptic neuron due to absence of MK2/3 is strongly correlated with this inability to acquire the new memories”.
Dr Corrêa argues that “Given their vital role in memory formation, MK2/3 pathways are important potential pharmaceutical targets for the treatment of cognitive deficits associated with ageing and dementia.”
http://www.nature.com/ncomms/2014/140819/ncomms5701/full/ncomms5701.html

Another stroke risk - NSFW

Be careful out there. From the Friendly Atheist blog;
http://www.patheos.com/blogs/friendlyatheist/2014/08/26/harlem-church-rails-against-obama-muslims-honorless-blacks-wishes-cancer-hiv-on-gay-friendly-believers/


Image © Rudie Kagie

Mahatma Gandhi — 'I like your Christ, I do not like your Christians. Your Christians are so unlike your Christ.'

Overweight causes hazardous inflammations

More empirical data about why you need to lose weight. Joyce Hoffman writes about that here also.

This kind of leads to wondering if the mini fasts that slow down Alzheimers would be connected to this response.

To Stave off Alzheimer’s, Stay Hungry?

Researchers: Mini-Fast Prevents Alzheimer's

But don't do these mini-fasts without your doctors prescription, damned dangerous they are.

Overweight causes hazardous inflammations

Researchers have found a possible molecular explanation for why overweight is harmful. This new knowledge may provide new drugs for heart attack, stroke, cancer and chronic intestinal inflammation.
“We believe that there is a connection between metabolism, inflammation, heart attack and stroke,” says Bente Halvorsen, professor at the Research Institute for Internal Medicine, University of Oslo, Norway. Together with the research group’s leader, Pål Aukrust, who last year received the university’s research award for his work on inflammatory diseases, and researcher Arne Yndestad, she has looked deeply into the molecular explanation of why overweight is harmful. “With this new knowledge, we can better understand why too much food can cause such serious diseases as heart attack, stroke, cancer and chronic intestinal inflammation.”
We eat too much
Malnutrition and insufficient nutrition lower the immune response, and this increases the risk of infections. If the immune defence system functioned normally, the body would respond with an inflammation to rid itself of the infection. When the immune defence system is impaired, the body is unable to defend itself through inflammation.
Overeating increases the immune response. This increased immune response causes the body to generate excessive inflammation, which may lead to a number of chronic diseases.
“It is therefore important to keep a balance. Too little and too much nutrition may both upset the immune defence system and increase the risk of disease.”
A number of diseases are caused by inflammation. Arthritis is a chronic inflammatory disease. Heart attack is an example of a disease that causes an acute and powerful inflammatory reaction.
“We can reduce the inflammatory reaction by losing weight. Some people risk never getting rid of the inflammation. We have attempted to understand what is needed to reduce the inflammatory reaction without having to lose weight,” Halvorsen explains.
Unfortunately, storage of energy causes an inflammatory reaction. The explanation lies in the close connection between the body’s immune system, energy conversion and the way in which we store energy. It can all be explained in terms of evolution. In our ancestors many hundred million years ago, this was all concentrated in one single organ, like in the modern-day fruit fly. Even though in humans this task is divided among three organs – the fatty tissue that stores energy, the liver that converts energy and the immune system – these organs still communicate closely with each other.
Evolutionarily speaking, humans are not made to eat so much on the contrary; they are intended to toil for their food.
“Mankind’s great challenge has consisted in obtaining sufficient food and surviving infections. Today, we rarely die of infections, but on the other hand we eat too much,” says Arne Yndestad.
Damage to the powerhouse in the cells
The researchers believe that overeating may cause stress to the mitochondria. The mitochondria are the cells’ powerhouses, converting fatty acids to energy.
Evolutionary biologists believe that mitochondria were bacteria that as life has developed have become an integrated part of our cells. The immune system may nevertheless perceive the mitochondria as foreign bodies. Much immunological research therefore focuses on the mitochondria.
When fatty acids accumulate in the cells, the mitochondria become stressed and gradually also damaged.
“When the cells receive excessive energy, the system starts to falter, and the engine may stall. Too much fatty acid causes an oxidative stress in the cells. We believe that long-term stress on the mitochondria may cause metaflammation. A metaflammation is a low-grade chronic inflammation over many years, and unfortunately it’s a condition that’s difficult to detect,” says Yndestad.
The body has its own defence system, called autophagy, which should eliminate damaged mitochondria. When we overeat, free fatty acids accumulate in the cells. This stresses the mitochondria. The stress in the cells causes damage to the mechanism that should eliminate the mitochondria.
When damaged mitochondria accumulate, the immune response is activated. This immune response is exactly what causes the inflammation.
Key signal molecules have been found
The UiO researchers, who also work at the new K.G. Jebsen Inflammation Research Centre, have studied some of the signal molecules inside the cells that trigger the inflammatory reaction. In other words, they have found one element of the energy conversion that may explain what happens when the mitochondria are dealing with the fatty acids. The special element, which is also an enzyme, has previously been studied in stroke patients.
“We believe that this enzyme can be regulated by overnutrition and that it is a key constituent in the inflammatory reaction. We have found that the plaque in the arteries of patients with arteriosclerosis contained a lot of this enzyme. When the plaque bursts, the patient may suffer a stroke,” Halvorsen points out.
In trials with mice, the researchers have tested what happens when the amount of this special enzyme is increased. It reduced the degree of arteriosclerosis.
Strengthening the theory
Their theory was strengthened when they studied how the absence of inflammasomes had an effect on heart function. Inflammasomes are part of the intra-cellular immune defence system.
“When the cells received excessive amounts of fatty acids, the inflammasomes were activated, causing an inflammation.”
Mice with heart attacks functioned better when the inflammasomes were removed.
“So this is about restoring the balance in the immune defence system”, says Yndestad .
A correlation with cancer
The researchers believe that their new discovery may also be a key mechanism in the development of cancer.
“Cancer cells need access to a lot of energy to divide. The cellular stress may transform cells to cancer. Studies of overweight may therefore give us a better understanding of cancer,” Halvorsen explains.
One who is particularly interested in this research is Professor Kristin Austlid Taskén at the Institute for Cancer Research.
“People who are overweight more often develop an aggressive variant of prostate cancer. Although the connection between overweight and cancer is well known, however, little is known about the mechanisms involved” Taskén says.
Her specialty is prostate cancer, a disease that strikes 5000 Norwegians each year.
“Since this is the most common form of cancer among men, it is essential to obtain more knowledge about the way in which overweight affects the metabolism of the cancer cells and leads to aggressive prostate cancer. For the cancer cells to be able to divide rapidly, they make use of new metabolic pathways that are quite unknown to us today. It is therefore useful to have more knowledge that can help us find new drugs that can dispose of the cancer cells,” Taskén points out to the research magazine Apollon.
http://www.apollon.uio.no/english/articles/2014/3_inflammations.h

Does “Time Is Brain” Also Mean “Time Is Clot”?

Damn, these idiots think that recanalization is the endpoint, it's not,
saving neurons is the endpoint. You damned idiots aren't even solving the right problem.   Solve the neuronal cascade of death.
http://stroke.ahajournals.org/content/45/9/2555.extract?etoc

Time Dependency of Tissue-Type Plasminogen Activator–Induced Recanalization in Acute Ischemic Stroke

1. Georgios Tsivgoulis, MD, PhD, MSc, FESO;
2. Andrei V. Alexandrov, MD

+ Author Affiliations

1. From the Second Department of Neurology, University of Athens, School of Medicine, “Attikon” University Hospital, Athens, Greece (G.T.); Department of Neurology, The University of Tennessee Health Science Center, Memphis (G.T., A.V.A.); and International Clinical Research Center, St. Anne’s University Hospital, Brno, Czech Republic (G.T.).

1. Correspondence to Andrei V. Alexandrov, MD, FAHA, Department of Neurology, The University of Tennessee Health Science Center, 855 Monroe Ave, Suite 415, Memphis, TN 38163. E-mail avalexandrov@att.net

Key Words:

• Editorial
• reperfusion
• stroke
• ultrasonography, Doppler, transcranial

See related article, p 2734.

Pooled analyses of major randomized controlled trials of intravenous thrombolysis (IVT) in acute ischemic stroke (AIS)^1–3 have established the clinical dictum of “Time is Brain”⁴ because longer times from stroke symptom onset to the initiation of IVT are associated with a lower likelihood of good clinical outcomes at 3 months. Recanalization could be the main mechanism why this time dependency is seen, and the so-called recanalization hypothesis is supported by evidence from a meta-analysis of clinical studies that documented recanalization.⁵ However, no prospective study to date has demonstrated that indeed shorter onset-to-treatment times (OTTs) result in shorter time to recanalization of an intracranial occlusion, in turn proving it to be the key link to better long-term functional outcomes. Conversely, could this also mean that longer times to treatment produce less recanalization attributable to clot maturation and progression of ischemic injury to brain tissues? Could “Time is Brain” also mean “Time is Clot”? As time is lost, clot wins.

In several pilot single-center studies of real-time monitoring of tissue-type plasminogen activator (tPA) infusion by transcranial Doppler (TCD), both the elapsed time from symptom onset to recanalization⁶ and the speed of clot lysis⁷ with IVT thrombolysis were associated with early clinical recovery from AIS as determined by serial National Institutes of Health Stroke Scale assessments. Nevertheless, the effect of the temporal profile of recanalization on 3-month functional outcome after adjusting for potential prognostic factors remains unknown.

In this issue …

[Full Text of this Article]

Association of Cognitive Functioning, Incident Stroke, and Mortality in Older Adults

I would never sponsor research that doesn't solve one of the problems in stroke, like this one. Man, we're wasting time and money doing these.
http://stroke.ahajournals.org/content/45/9/2563.abstract?etoc

1. Kumar B. Rajan, PhD;
2. Neelum T. Aggarwal, MD;
3. Robert S. Wilson, PhD;
4. Susan A. Everson-Rose, PhD, MPH;
5. Denis A. Evans, MD

+ Author Affiliations

1. From the Rush Institute for Healthy Aging, Department of Internal Medicine (K.B.R., D.A.E.), Rush Alzheimer’s Disease Center (N.T.A., R.S.W.), Department of Neurological Sciences (N.T.A., R.S.W.), and Department of Behavioral Sciences (R.S.W.), Rush University Medical Center, Chicago, IL; and Department of Medicine, University of Minnesota, Minneapolis (S.A.E.-R.).

1. Correspondence to Kumar B. Rajan, PhD, Department of Internal Medicine, Rush University Medical Center, 1645 W Jackson Blvd, Suite 675, Chicago, IL 60612. E-mail kumar_rajan@rush.edu

Abstract

Background and Purpose—Stroke increases the risk of dementia; however, bidirectional association of incident stroke and cognitive decline below dementia threshold is not well established. Also, both cognitive decline and stroke increase mortality risk.

Methods—A longitudinal population-based cohort of 7217 older adults without a history of stroke from a biracial community was interviewed at 3-year intervals. Cognitive function was assessed using a standardized global cognitive score. Stroke was determined by linkage with Medicare claims, and mortality was ascertained via the National Death Index. We used a Cox model to assess the risk of incident stroke, a joint model with a piecewise linear mixed model with incident stroke as a change point for cognitive decline process, and a time-dependent relative risk regression model for mortality risk.

Results—During follow-up, 1187 (16%) subjects had incident stroke. After adjusting for known confounders, lower baseline cognitive function was associated with a higher risk of incident stroke (hazard ratio, 1.61; 95% confidence interval, 1.46–1.77). Cognitive function declined by 0.064 U per year before incident stroke occurrence and 0.122 U per year after stroke, a nearly 1.9-fold increase in cognitive decline (95% confidence interval, 1.78–2.03). Both stroke (hazard ratio, 1.17; 95% confidence interval, 1.08–1.26) and cognitive decline (hazard ratio, 1.90; 95% confidence interval, 1.81–1.98) increased mortality risk.

Conclusions—Baseline cognitive function was associated with incident stroke. Cognitive decline increased significantly after stroke relative to before stroke. Cognitive decline increased mortality risk independent of the risk attributable to stroke and should be followed as a marker for both stroke and mortality.

Trends in 10-Year Survival of Patients With Stroke Hospitalized Between 1980 and 2000 - Minnesota

This really doesn't help much because we have no objective damage diagnoses from the stroke so we could compare year by year whether our stroke teams are doing better in applying tPA and stopping the neuronal cascade of death.  This reduction probably has almost nothing to do with doctor interventions.  If you don't know what the problem is, you'll never be able to solve it.
http://stroke.ahajournals.org/content/45/9/2575.abstract?etoc

The Minnesota Stroke Survey

1. Kamakshi Lakshminarayan, MD, PhD;
2. Alan K. Berger, MD, MS;
3. Candace C. Fuller, PhD, MPH;
4. David R. Jacobs Jr, PhD;
5. David C. Anderson, MD;
6. Lyn M. Steffen, PhD;
7. Arthur Sillah, MPH;
8. Russell V. Luepker, MD, MS

+ Author Affiliations

1. From the Division of Epidemiology and Community, School of Public Health (K.L., D.R.J., L.M.S., R.V.L.), Department of Medicine, Division of Interventional Cardiology (A.K.B.), and Department of Neurology, Medical School (D.C.A.), University of Minnesota, Minneapolis; Department of Population Medicine, Harvard Medical School and Harvard Pilgrim HealthCare Institute, Boston, MA (C.C.F.); and Division of Applied Research, Allina Health, Minneapolis, MN (A.S.).

1. Correspondence to Kamakshi Lakshminarayan, MD, PhD, Division of Epidemiology and Community Health, School of Public Health, University of Minnesota, 1300 S Second St, Suite 300, Minneapolis, MN 55454-1015. E-mail laksh004@umn.edu

Abstract

Background and Purpose—We report on trends in poststroke survival, both in the early period after stroke and over the long term. We examine these trends by stroke subtype.

Methods—The Minnesota Stroke Survey is a study of all hospitalized patients with acute stroke aged 30 to 74 years in the Minneapolis–St Paul metropolis. Validated stroke events were sampled for survey years 1980, 1985, 1990, 1995, and 2000 and subtyped as ischemic or hemorrhagic by neuroimaging for survey years 1990, 1995, and 2000. Survival was obtained by linkage to vital statistics data through the year 2010.

Results—There were 3773 acute stroke events. Age-adjusted 10-year survival improved from 1980 to 2000 (men 29.5% and 46.5%; P<0.0001; women 32.6% and 50.5%; P<0.0001). Ten-year ischemic stroke survival (n=1667) improved from 1990 to 2000 (men 35.3% and 50%; P=0.0001; women 38% and 55.3%; P<0.0001). Ten-year hemorrhagic stroke survival showed a trend toward improvement, but this (n=489) did not reach statistical significance, perhaps because of their smaller number (men 29.7% and 45.8%; P=0.06; women 39.2% and 49.6%; P=0.2). Markers of stroke severity including unconsciousness or major neurological deficits at admission declined from 1980 to 2000 while neuroimaging use increased.

Conclusions—These poststroke survival trends are likely because of multiple factors, including more sensitive case ascertainment shifting the case mix toward less severe strokes, improved stroke care and risk factor management, and overall improvements in population health and longevity.

The way we think about charity is dead wrong

This can be applied so appallingly truthfully to our stroke associations. Look at the results our stroke associations have given us. NOTHING!!!  Nothing on understanding and repeating neuroplasticity. Nothing on solving fatigue and spasticity. Nothing on fast, easy and objective diagnosis of strokes.
http://www.ted.com/talks/dan_pallotta_the_way_we_think_about_charity_is_dead_wrong?
Activist and fundraiser Dan Pallotta calls out the double standard that drives our broken relationship to charities. Too many nonprofits, he says, are rewarded for how little they spend — not for what they get done. Instead of equating frugality with morality, he asks us to start rewarding charities for their big goals and big accomplishments (even if that comes with big expenses). In this bold talk, he says: Let's change the way we think about changing the world.

Modeling Immunity and Inflammation in Stroke Can Mice Be Trusted?

Sounds like a researcher problem to solve.
http://stroke.ahajournals.org/content/45/9/e177.extract?etoc

1. Ulrich Dirnagl, MD

+ Author Affiliations

1. From the Departments of Neurology and Experimental Neurology Charité, Center for Stroke Research Berlin, Charité, ExcellenceCluster NeuroCure–Universitätsmedizin Berlin, Berlin, Germany; German Center for Neurodegenerative Diseases (DZNE), Partner Site, Berlin, Germany; and German Center for Cardiovascular Diseases (DZHK), Partner Site, Berlin, Germany.

1. Correspondence to Ulrich Dirnagl, MD, Center for Stroke Research Berlin, Charité Universitätsmedizin Berlin, Charitéplatz 1, 10117 Berlin, Germany. E-mail ulrich.dirnagl@charite.de

Key Words:

• immune system
• inflammation
• models, animal
• stroke

Introduction

Sixty-five million years have passed since mouse and man shared a common ancestor. The principles of evolution, as well as the scientific literature, suggest that there are many similarities between both mammal species but also significant differences. Humans are definitely no 75 kg mice,¹ but is it true that “the mouse model has been totally misleading for at least three major killers—sepsis, burns, and trauma,” as the New York Times concluded after the publication of a study by Seok et al?² By looking at transcriptional responses of blood cells, this study found “that, although acute inflammatory stresses from different etiologies result in highly similar genomic responses in humans, the responses in corresponding mouse models correlate poorly with the human conditions and also, one another.”

The results of the Seok et al² study are by no means surprising or new,³ but they nevertheless carry an important message for experimental stroke research. The authors used male mice of the C57 BL/6J strain, which is exquisitely resistant to sepsis: more than one million-fold doses of endotoxin are required to cause shock in this mouse strain. The mice are inbred and raised under specific pathogen-free conditions, so at the time of the study, the 8-week-old mice had a naive and immature immune system.

In contrast, rodents are as sensitive to focal cerebral ischemia as humans. The evolution of the infarct and surrounding penumbra has similar temporal and histopathologic dynamics, and the time windows for thrombolysis after embolic stroke are practically …

[Full Text of this Article]

TeleStroke Units Serving as a Model of Care in Rural Areas -Germany/Bavaria

I absolutely hate these articles. They are just puff pieces meant to distract from all the actual f*cking failures in stroke.
http://stroke.ahajournals.org/content/45/9/2739.abstract?etoc

10-Year Experience of the TeleMedical Project for Integrative Stroke Care

1. Peter Müller-Barna, MD*;
2. Gordian J. Hubert, MD*;
3. Sandra Boy, MD;
4. Ulrich Bogdahn, MD;
5. Silke Wiedmann, PhD;
6. Peter U. Heuschmann, MD, MPH;
7. Heinrich J. Audebert, MD

+ Author Affiliations

1. From the Department of Neurology, Klinikum Harlaching, Städtisches Klinikum München GmbH, München, Germany (P.M.-B., G.J.H.); Department of Neurology, Krankenhaus Agatharied, Hausham, Germany (P.M.-B.); Department of Neurology, University Hospital Regensburg, Regensburg, Germany (S.B., U.B.); Institute of Clinical Epidemiology and Biometry (S.W., P.U.H.) and Comprehensive Heart Failure Center (S.W., P.U.H.), University of Würzburg, Würzburg, Germany; Clinical Trial Center Würzburg, University Hospital Würzburg, Würzburg, Germany (S.W., P.U.H.); and Klinik und Hochschulambulanz für Neurologie (H.J.A.) and Center for Stroke Research (H.J.A.), Charité–Universitätsmedizin Berlin, Berlin, Germany.

1. Correspondence to Peter Müller-Barna, MD, Department of Neurology, Krankenhaus Agatharied, Norbert-Kerkel-Platz, 83734 Hausham, Germany. E-mail peter.mueller-barna@khagatharied.de

1. ↵* Drs Müller-Barna and Hubert contributed equally.

Abstract

Background and Purpose—Stroke Unit care improves stroke prognosis and is recommended for all patients with stroke. In rural areas, population-wide implementation of Stroke Units is challenging. Therefore, the TeleMedical Project for integrative Stroke Care (TEMPiS) was established in 2003 as a TeleStroke Unit network to overcome this barrier in Southeast Bavaria/Germany. Evaluation of its implementation between 2003 and 2005 had revealed improved process quality and clinical outcomes compared with matched hospitals without TeleStroke Units. Data on sustainability of these effects are lacking.

Methods—Effects on the stroke care of the local population were analyzed by using data from official hospital reports. Prospective registries from 2003 to 2012 describe processes and outcomes of consecutive patients with stroke and transient ischemic attack treated in TEMPiS hospitals. Quality indicators assess diagnostics, treatment, and outcome. Rates and timeliness of intravenous thrombolysis as well as data on teleconsultations and secondary interhospital transfers were reported over time.

Results—Within the covered area, network implementation increased the number of patients with stroke and transient ischemic attack treated in hospitals with (Tele-)Stroke Units substantially from 19% to 78%. Between February 2003 and December 2012, 54 804 strokes and transient ischemic attacks were treated in 15 regional hospitals, and 31 864 teleconsultations were performed. Intravenous thrombolysis was applied 3331 stroke cases with proportions increasing from 2.6% to 15.5% of all patients with ischemic stroke. Median onset-to-treatment times decreased from 150 (interquartile range, 127–163) to 120 minutes (interquartile range, 90–160) and door-to-needle times from 80 (interquartile range, 68–101) to 40 minutes (interquartile range, 29–59).

Conclusions—TeleStroke Units can provide sustained high-quality stroke care in rural areas.

Computed Tomographic Angiography and Cerebral Blood Volume Can Predict Final Infarct Volume and Outcome After Recanalization

These idiots still don't have a clue that the neuronal cascade of death keeps on killing neurons even after recanalization.
Some day there are going to be dozens on researchers working on that and they'll wonder why they took so long to understand the etiology of stroke damage. 

Computed Tomographic Angiography and Cerebral Blood Volume Can Predict Final Infarct Volume and Outcome After Recanalization

1. Cheemun Lum, MD, FRCP;
2. Muhammad Ejaz Ahmed, MBBS;
3. Satya Patro, MBBS;
4. Rebecca Thornhill, PhD;
5. Matthew Hogan, MD, FRCP;
6. Daniela Iancu, MD;
7. Howard Lesiuk, MD, FRCS;
8. Marlise dos Santos, MD, MSc;
9. Dar Dowlatshahi, MD, PhD, FRCPC;
10. on behalf of the Ottawa Stroke Research Group (OSRG)

+ Author Affiliations

1. From the Interventional Neuroradiology Section, Department of Medical Imaging-Diagnostic (C.L., M.E.A., S.P., R.T., D.I., H.L., M.d.S.) and Division of Neurology, Department of Medicine (M.H., D.D.), The Ottawa Hospital, Ottawa Hospital Research Institute (OHRI), University of Ottawa, Ottawa, Ontario, Canada.

1. Correspondence to Cheemun Lum, MD, C1-Diagnostic Imaging, Civic Campus, The Ottawa Hospital, 1053 Carling Ave, Ottawa, Ontario, Canada K1Y 4E9. E-mail chlum@ottawahospital.on.ca

Abstract

Background and Purpose—Recanalization rates are higher in acute anterior stroke treated with stent-retrievers when compared with older techniques. However, some still have sizeable infarcts and poor outcome. This may be related to underestimation of core infarct on nonenhanced computed tomography (NECT). CT angiography (CTA) source images (CTASI) and CT perfusion may be more informative. We hypothesize that core infarct estimation with NECT, CTA, and CT perfusion predicts infarct at 24 hours and outcome after fast recanalization.

Methods—Consecutive good recanalization patients with proximal anterior circulation stroke were evaluated. We assessed Alberta Stroke Program Early CT Score (ASPECTs) on NECT for subtle early infarct, hypodensity, loss of gray–white (CTASI), and low cerebral blood volume (CBV; CT perfusion). Sensitivity and specificity for predicting infarct by region were calculated.

Results—Of 46 patients, 36 (78%) had successful thrombectomy. Median ASPECTS was 10 for NECT early infarct and frank hypodensity; for CBV, CTASI-ASPECTS was 8. CTASI had the highest sensitivity of 71% and specificity of 82% for 24 hours NECT infarct. There was moderate correlation and concordance between CBV/24-hour NECT (R_p=0.51; R_c=0.50) and CTASI/24-hour NECT (R_p=0.54 and R_c=0.53). Thirty-four patients (74%) had good outcomes. Median ASPECTS was higher on CTASI (8 versus 5; P=0.04) and CBV (9 versus 5; P=0.03) for patients with good versus bad outcome. There were better outcomes with increasing CTASI-ASPECTS (P=0.004) and CBV-ASPECTS (P=0.02).

Conclusions—CTASI and CBV were better at predicting 24-hour infarct and outcome than NECT. Appropriate advanced imaged guided selection may improve outcomes in large-vessel stroke treated with the newest techniques.

Effect of Bhramari pranayama and OM chanting on pulmonary function in healthy individuals: A prospective randomized control trial

And no explanation from supposedly smart researchers. The reason this works is because of the NO - nitric oxide generated by chanting.
Failure at a large scale. Their research leaders should be ashamed of themselves for not knowing this.

Nobel Prize Awarded to Scientists for Nitric Oxide Discoveries

 

Do you think that maybe this might be helpful immediately post-stroke? Never do this if your doctor doesn't know about this. Breathing hard is dangerous if it is not prescribed and you would show that you know more than your doctor.

Inhalation of nitric oxide could help improve blood flow to ischemic brain 

 

How to create NO here:

Strong humming for one hour daily to terminate chronic rhinosinusitis in four days : A case report and hypothesis for action by stimulation of endogenous nasal nitric oxide production

 

 

http://www.ncbi.nlm.nih.gov/pubmed/25035619

Mooventhan A¹, Khode V².

Author information

Abstract

BACKGROUND/AIM:

Yoga is an ancient Indian science as well as the way of life. Pranayama is a part of yoga, which improves pulmonary function in combination of many pranayama, but the aim of our study is to evaluate the effect of only Bhramari pranayama and OM chanting on pulmonary function in healthy individuals.

MATERIALS AND METHODS:

A total of 82 subjects were randomized into the study group (SG) (n = 41) and control group (CG) (n = 41). Baseline assessment was performed before intervention for both groups. SG practiced Bhramari pranayama and OM chanting for the duration of 10 min (5 min for each practice)/day for the period of 6 days/week for 2 weeks and CG did not practice so. After intervention post-assessment was performed for SG (n = 40) and CG (n = 39). Statistical analysis was performed by Independent samples t-test and Student's paired t-test with the use of Statistical Package for the Social Sciences version 16 (2007, USA).

RESULTS:

The result showed a significant improvement in peak expiratory flow (PEF), forced expiratory flow (FEF)25% and maximal voluntary ventilation (MVV) along with a significant reduction in weight in SG compared with CG in independent samples t-test. Significant improvement in slow vital capacity (SVC), forced expired volume in 1 s (FEV1) along with PEF, FEF25% and MVV; Significant reduction in weight and body mass index were observed in SG unlike in CG in Student's paired t-test. No significant changes were found in forced vital capacity, FEV1 /SVC and FEF50% , between and within the group analysis of SG and CG.

CONCLUSION:

Bhramari pranayama and OM chanting are effective in improving pulmonary function in healthy individuals.

A strong medical research future - Australia

This is good, but you survivors will need to contact him directly and have him focus on solving the problems in stroke. With 

1 in 4 per WHO that has a stroke

, this is a major unmet need.
http://blog.neura.edu.au/2014/08/25/ed-message/?utm_source=rss&utm_medium=rss&utm_campaign=ed-message

Professor Peter Schofield is the Executive Director of NeuRA - See more at: http://blog.neura.edu.au/author/schofield/#sthash.RZ92xmbY.dpuf

 Professor Peter Schofield is the Executive Director of NeuRA

Problems in stroke;

1. There is no fast, easy and objective way to diagnose a stroke. Maybe when the Qualcomm Tricorder X Prize is available. A number of friends have waited hours in ERs until stroke symptoms have visibly manifested themselves.
http://oc1dean.blogspot.com/2013/11/34-teams-are-building-medical.html

2. Only 10% get to almost full recovery.
http://www.ninds.nih.gov/disorders/stroke/stroke_rehabilitation.htm
3. 12% tPA efficacy
http://wrkf.org/post/more-stroke-patients-now-get-clot-busting-drug
4. Nothing being done to stop the neuronal cascade of death during the first week.
http://newswire.rockefeller.edu/2009/01/15/discovery-could-help-scientists-stop-the-death-cascade-after-a-stroke/
5. No one knows how to cure spasticity.
6.  No one knows how to cure fatigue.
7. F.A.S.T is actually a failure because even at its best tPA is only delivered to 33% of those eligible and then of those that get it  it only works to completely reverse the stroke 12% of the time.

Professor Peter Schofield is the Executive Director of NeuRA - See more at: http://blog.neura.edu.au/author/schofield/#sthash.RZ92xmbY.dpuf

Management of Stroke Rehabilitation (2010)

From the VA, you will need to have your doctor compare these guidelines to whatever crap they have at their hospital, Then publish the failings in the local paper. Maybe embarrassment is the only way to actually get some stroke protocols that work. Everything else has been a failure. 
http://www.healthquality.va.gov/guidelines/rehab/stroke/
This is actually a f*cking failure also. This next sentence means that every single person involved with this basically threw up their hands and said they didn't know how to handle stroke cases.

Although the reviews and trials make it clear that rehabilitation is a dominant component of organized services, it is not possible  to specify precise standards and protocols 

for specific types of specialized units for stroke patients. 

 Only 152 pages of worthless guidelines. There must be dozens of supposedly highly educated people that wrote this crap.
Once again the stroke medical world is waiting for someone else to solve the problems in stroke. Damn lazy assholes. I would have fired everyone of them for dereliction of duty or not meeting goals.