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 438 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:

Tuesday, November 24, 2015

Effects of golden hour thrombolysis: a Prehospital Acute Neurological Treatment and Optimization of Medical Care in Stroke (PHANTOM-S) substudy

I couldn't really tell from this if the reason better outcomes were observed was because the intervention was delivered fast enough not to trigger the neuronal cascade of death.  If we don't know what that time cutoff is then we don't know what the goal should be. And all these problems could be eliminated if we followed up on research to have a fast, easy and objective diagnosis with no neurologist involvement.
Test out these 17 diagnosis possibilities to find out which one is the best?  Or maybe the Qualcomm Xprize for the tricorder?



The effectiveness of intravenous thrombolysis in acute ischemic stroke is time dependent. The effects are likely to be highest if the time from symptom onset to treatment is within 60 minutes, termed the golden hour.


To determine the achievable rate of golden hour thrombolysis in prehospital care and its effect on outcome. (Wrong objective; should be better recovery results)


The prospective controlled Prehospital Acute Neurological Treatment and Optimization of Medical Care in Stroke study was conducted in Berlin, Germany, within an established infrastructure for stroke care. Weeks were randomized according to the availability of a specialized ambulance (stroke emergency mobile unit (STEMO) from May 1, 2011, through January 31, 2013. We included 6182 consecutive adult patients for whom a stroke dispatch (44.1% male; mean [SD] age, 73.9 [15.0] years) or regular care (45.0% male; mean [SD] age, 74.2 [14.9] years) were included.


The STEMO was deployed when the dispatchers suspected an acute stroke during emergency calls. If STEMO was not available (during control weeks, when the unit was already in operation, or during maintenance), patients received conventional care. The STEMO is equipped with a computed tomographic scanner plus a point-of-care laboratory and telemedicine connection. The unit is staffed with a neurologist trained in emergency medicine, a paramedic, and a technician. Thrombolysis was started in STEMO if a stroke was confirmed and no contraindication was found.


Rates of golden hour thrombolysis, 7- and 90-day mortality, secondary intracerebral hemorrhage, and discharge home.


Thrombolysis rates in ischemic stroke were 200 of 614 patients (32.6%) when STEMO was deployed and 330 of 1497 patients (22.0%) when conventional care was administered (P < .001). Among all patients who received thrombolysis, the proportion of golden hour thrombolysis was 6-fold higher after STEMO deployment (62 of 200 patients [31.0%] vs 16 of 330 [4.9%]; P < .01). Compared with patients with a longer time from symptom onset to treatment, patients who received golden hour thrombolysis had no higher risks for 7- or 90-day mortality (adjusted odds ratios, 0.38 [95% CI, 0.09-1.70]; P = .21 and 0.69 [95% CI, 0.32-1.53]; P = .36) and were more likely to be discharged home (adjusted odds ratio, 1.93 [95% CI, 1.09-3.41]; P = .02).


The use of STEMO increases the percentage of patients receiving thrombolysis within the golden hour. Golden hour thrombolysis entails no risk to the patients' safety and is associated with better short-term outcomes. (Tell us what those better results were)

TRIAL REGISTRATION: Identifier: NCT01382862.

Four key studies that link coffee to heart attacks and hypertension

This seems to follow the same course as alcohol consumption. Only those with the proper genetic marker benefit. But your doctor will unlikely ever do gene testing prior to telling you coffee is bad for you because it raises your blood pressure. I most assuredly will not get gene testing to see if I'm in the right category.
Is drinking coffee good for you? Some research indicates that that simple question cannot be answered without knowing something about your DNA.
Maybe the clearest evidence that genetics determines caffeine metabolism arises from a study of twins, published in 2002, that indicates that the speed with which a person processes caffeine is largely heritable.
At the same time, other studies have identified a single nugget of our DNA that seems to determine whether we process caffeine quickly or slowly. That, in turn, appears to have a large effect on whether coffee is good for your health.
For those who process caffeine slowly, this line of research indicates, drinking coffee raises the risks of heart attacks and high blood pressure. For those who process it quickly, drinking coffee seems to be safe - it may even protect against a heart attack or high blood pressure.
While researchers caution that more work needs to be done, they suggest that giving the public a general guideline regarding coffee doesn’t make sense. People are too different.
Here are some of the highlights in this line of research.
For the key studies in favor of coffee, try this.
“The interindividual differences in the 3-demethylation of caffeine alias CYP1A2 is determined by both genetic and environmental factors.”
Pharmacogenetics, August 2002.
Finding: Forty-nine identical twins and 34 fraternal twins were given 200 milligrams of caffeine; six hours later, a urine sample was taken. Those sample were then analyzed to see how quickly each person had broken down, or metabolized, the caffeine. In identical twins, the rates of metabolism were about twice as correlated as they were in fraternal twins. The scientists concluded that genetics largely determines the rate at which a person processes caffeine.
“CYP1A2 phenotype and genotype in a population from the Carboniferous Region of Coahuila, Mexico.”
Toxicology Letters, April 2005
Finding: Scientists in Mexico gave 46 volunteers a cup of instant coffee containing 140 milligrams of caffeine. Eight hours later, urine samples were collected. Those subjects who had one variant of the CYP1A2 gene processed caffeine more than twice as quickly as those who had the other, researchers found. Other similar efforts in China and Germany found a link between the gene and caffeine metabolism, predominantly in smokers.
“Coffee, CYP1A2 Genotype, and Risk of Myocardial Infarction”
JAMA, March 2006
Finding: Researchers compared about 2,000 people in Costa Rica who had a heart attack with 2,000 others who had not, examining both how much coffee they drank, as well as their DNA. In those subjects with the genetic marker indicating slow caffeine metabolism, the chance of heart attack appeared to rise with each cup of coffee. By contrast, those subjects with the genetic marker for rapid caffeine metabolism had a lower chance of heart attack with each cup.
The authors concluded: “Intake of coffee was associated with an increased risk of nonfatal [heart attack] only among individuals with slow caffeine metabolism, suggesting that caffeine plays a role in this association.”
“CYP1A2 genotype modifies the association between coffee intake and the risk of hypertension”
Journal of Hypertension, August 2009.
Finding: Researchers looked at the genetics, blood pressure and coffee habits of 553 young Italian over more than eight years. As with heart attacks (see above), the effects of coffee diverged depending on a person’s genetics.
For those with the gene for slow caffeine metabolism, the risks of high blood pressure rose dramatically with coffee intake. For those with the gene for rapid caffeine metabolism, the risk of high blood pressure dropped with coffee intake.
The authors concluded: People with the slower caffeine metabolism “are at increased risk and should thus abstain from coffee.” On the other hand, people with the genetics for the rapid caffeine metabolism “can safely drink coffee.”

Monday, November 23, 2015

Modafinil May Alleviate Poststroke Fatigue

The primary results do not correspond to the title. Whomever wrote the title is lying.
Maybe you want modafinil for this use:

Systematic review shows ‘smart drug’ modafinil does enhance cognition

or this:

Effects of modafinil on non-verbal cognition, task enjoyment and creative thinking in healthy volunteers


Modafinil May Alleviate Poststroke Fatigue

A Randomized, Placebo-Controlled, Double-Blinded Trial

  1. Rune Skovgaard Rasmussen, MA, PhD
+ Author Affiliations
  1. Departments of Neurology (M.B.P., K.O., R.S.R.), Radiology (B.D.), and Clinical Physiology (B.Z.), Herlev University Hospital, Herlev, Denmark; and Department of Radiology, Hilleroed University Hospital, Hilleroed, Denmark (B.D.).
  1. Correspondence to Mai Bang Poulsen, MD, Department of Neurology, Herlev Hospital, Herlev Ringvej 75, 2730 Herlev, Denmark. E-mail


Background and Purpose—Poststroke fatigue is common and reduces quality of life. Current evidence for intervention is limited, and this is the first placebo-controlled trial to investigate treatment of poststroke fatigue with the wakefulness promoting drug modafinil.
Methods—The trial was randomized, double-blinded, and placebo-controlled. Patients were treated with 400-mg modafinil or placebo for 90 days. Assessments were done at inclusion, 30, 90, and 180 days. The primary end point was fatigue at 90 days measured by the Multidimensional Fatigue Inventory-20 general fatigue domain. Secondary end points included the Fatigue Severity Scale, the Montreal Cognitive Assessment, the modified Rankin Scale and the Stroke-specific quality of Life questionnaire. Adult patients with a recent stroke achieving a score of ≥12 on the Multidimensional Fatigue Inventory-20 general fatigue domain were consecutively included. Exclusion criteria were severe cognitive disabilities and contraindications for modafinil treatment.
Results—One thousand one hundred twenty-one patients with stroke were screened and 41 patients included, 21 received modafinil. The primary end point, the Multidimensional Fatigue Inventory-20 general fatigue score, did not differ between groups. Patients in the modafinil group obtained better scores on the Fatigue Severity Scale (P=0.02) and in some subscales of the stroke-specific quality of life questionnaire (0.001<P<0.05), which were secondary outcomes. No serious adverse reactions were observed and there was no difference in blood pressure between groups.
Conclusions—There were no significant differences between the 2 groups with regard to the primary end point. There were secondary significant outcomes that should be explored in future trials.
Clinical Trial Registration—URL: Unique identifier: NCT01800097.

Does stroke location predict walk speed response to gait rehabilitation?

Well shit, Is water wet?

  1. P. Simon Jones1,
  2. Valerie M. Pomeroy2,
  3. Jasmine Wang3,
  4. Gottfried Schlaug3,
  5. S. Tulasi Marrapu1,
  6. Sharon Geva1,
  7. Philip J. Rowe4,
  8. Elizabeth Chandler2,
  9. Andrew Kerr4,
  10. Jean-Claude Baron1,5,* and
  11. for the SWIFT-Cast investigators
Article first published online: 19 NOV 2015
DOI: 10.1002/hbm.23059

  1. Conflicts of Interest: None.



  • MRI;
  • voxel-based lesion–symptom mapping;
  • cortico-spinal tract;
  • ambulation;
  • recovery



Recovery of independent ambulation after stroke is a major goal. However, which rehabilitation regimen best benefits each individual is unknown and decisions are currently made on a subjective basis.(Everything in stroke should be objective) Predictors of response to specific therapies would guide the type of therapy most appropriate for each patient. Although lesion topography is a strong predictor of upper limb response, walking involves more distributed functions. Earlier studies that assessed the cortico-spinal tract (CST) were negative, suggesting other structures may be important.
Experimental Design: The relationship between lesion topography and response of walking speed to standard rehabilitation was assessed in 50 adult-onset patients using both volumetric measurement of CST lesion load and voxel-based lesion–symptom mapping (VLSM) to assess non-CST structures. Two functional mobility scales, the functional ambulation category (FAC) and the modified rivermead mobility index (MRMI) were also administered. Performance measures were obtained both at entry into the study (3–42 days post-stroke) and at the end of a 6-week course of therapy. Baseline score, age, time since stroke onset and white matter hyperintensities score were included as nuisance covariates in regression models.
Principal Observations: CST damage independently predicted response to therapy for FAC and MRMI, but not for walk speed. However, using VLSM the latter was predicted by damage to the putamen, insula, external capsule and neighbouring white matter.


Walk speed response to rehabilitation was affected by damage involving the putamen and neighbouring structures but not the CST, while the latter had modest but significant impact on everyday functions of general mobility and gait. Hum Brain Mapp, 2015.

Problem-Solving Therapy During Outpatient Stroke Rehabilitation Improves Coping and Health-Related Quality of Life

So rather than finding recovery solutions for survivors we have persons researching coping skills. You wouldn't need so many fucking coping skills if you solved the goddamned problems in stroke. God I hate stupid people.

Randomized Controlled Trial

  1. Gerard M. Ribbers, MD, PhD
+ Author Affiliations
  1. From the Department of Rehabilitation Medicine (M.M.V., M.H.H.-K., G.M.R.) and Department of Psychiatry, Section Medical Psychology and Psychotherapy (A.v.S., J.J.V.B.), Erasmus University Medical Center, Rotterdam, The Netherlands; Rotterdam Neurorehabilitation Research Department (RoNeRes), Rijndam Rehabilitation Center, Rotterdam, The Netherlands (M.M.V., M.H.H.-K., G.M.R.); and Department of Physical and Rehabilitation Medicine, Ghent University Hospital, Ghent, Belgium (E.L.).
  1. Correspondence to Majanka H. Heijenbrok-Kal, PhD, Rotterdam Neurorehabilitation Research (RoNeRes), Rijndam Rehabilitation Center, PO Box 23181, 3001 KD, Rotterdam, The Netherlands. E-mail


Background and Purpose—This study investigated whether problem-solving therapy (PST) is an effective group intervention for improving coping strategy and health-related quality of life (HRQoL) in patients with stroke .
Methods—In this multicenter randomized controlled trial, the intervention group received PST as add-on to standard outpatient rehabilitation, the control group received outpatient rehabilitation only. Measurements were performed at baseline, directly after the intervention, and 6 and 12 months later. Data were analyzed using linear-mixed models. Primary outcomes were task-oriented coping as measured by the Coping Inventory for Stressful Situations and psychosocial HRQoL as measured by the Stroke-Specific Quality of Life Scale. Secondary outcomes were the EuroQol EQ-5D-5L utility score, emotion-oriented and avoidant coping as measured by the Coping Inventory for Stressful Situations, problem-solving skills as measured by the Social Problem Solving Inventory-Revised, and depression as measured by the Center for Epidemiological Studies Depression Scale.
Results—Included were 166 patients with stroke, mean age 53.06 years (SD, 10.19), 53% men, median time poststroke 7.29 months (interquartile range, 4.90–10.61 months). Six months post intervention, the PST group showed significant improvement when compared with the control group in task-oriented coping (P=0.008), but not stroke-specific psychosocial HRQoL. Furthermore, avoidant coping (P=0.039) and the utility value for general HRQoL (P=0.034) improved more in the PST group than in the control after 6 months.
Conclusions—PST seems to improve task-oriented coping but not disease-specific psychosocial HRQoL after stroke >6-month follow-up. Furthermore, we found indications that PST may improve generic HRQoL recovery and avoidant coping.
Clinical Trial Registration—URL: Unique identifier: CNTR2509.

Mechanisms and Functional Significance of Stroke-induced Neurogenesis

If I had a 'good' stroke doctor I would expect that person to have read this and updated stroke protocols within a week. Then contacting every single stroke patient of theirs to inform them of the good news. But I bet there isn't one single 'good' stroke doctor in the world. Not even great, just 'good'.  Doing that is the minimum I would expect from my doctor,. anything else should be a fireable offense.

  • 1GIGA-Neurosciences, University of liège, Belgium
Stroke affects one in every six people worldwide, and is the leading cause of adult disability. After stroke, some limited spontaneous recovery occurs, the mechanisms of which remain largely unknown. Multiple, parallel approaches are being investigated to develop neuroprotective, reparative and regenerative strategies for the treatment of stroke. For years, clinical studies have tried to use exogenous cell therapy as a means of brain repair, with varying success. Since the rediscovery of adult neurogenesis and the identification of adult neural stem cells in the late nineties, one promising field of investigation is focused upon triggering and stimulating this self-repair system to replace the neurons lost following brain injury. For instance, it is has been demonstrated that the adult brain has the capacity to produce large numbers of new neurons in response to stroke. The purpose of this review is to provide an updated overview of stroke-induced adult neurogenesis, from a cellular and molecular perspective, to its impact on brain repair and functional recovery.

Feeling grateful for you today - National Stroke Association email

I'm not grateful for the NSA. Reasoning below in red. And Matt Lopez is even a stroke survivor and should know better.
Dear dean,
Matt Lopez
Come Back Strong Blue White
As 2015 comes to a close, I am excited about the lives that have been saved and impacted by the work of National Stroke Association. This year, we launched Stroke Recover Navigator—a game-changer for anyone who has experienced the life-altering effects of a stroke. This impactful program helps stroke survivors in those confusing and frightening first few months when they have left the hospital and are trying to make sense of their new life. Then, this summer, Come Back Strong was unveiled. With the launch of the Come Back Strong movement, our goal is to provide stroke survivors with hope after stroke so they can begin their journey to recovery and Come Back Strong. Have you gotten involved with the Come Back Strong movement yet? This Come Back Strong initiative wouldn't be  necessary if you would create protocols that get survivors back to 100% recovery. More important if you solved and prevented the neuronal cascade of death. You aren't even solving the problems out there. You're trying to ameliorate the aftereffects. Damn it all, use some of your fucking neurons and understand cause and effect.
This year, I am so grateful for your support.
I am giving thanks this year to you. We have a passion for increasing awareness of life-saving stroke information, improving quality of life for stroke survivors and caregivers, and impacting survivor empowerment. Because of you, this important work will continue.
The next year is going to be exciting. We look forward to sharing with you more new resources and programs that continue to reduce the incidence of stroke and improve your quality of life. You have told us what your greatest needs are(Really, I haven't been contacted) and we look forward to continuing to meet those needs.
Thank you for trusting us to be the voice of the stroke community. I don't trust you because you have no outreach to survivors. Look at what a great stroke association would be doing for outreach.
With thanks,
signed by Matt Lopez, CEO
Matt Lopez
CEO, Stroke Survivor
National Stroke Association

Sunday, November 22, 2015

If you haven't done the reading, why expect to be treated as a stroke professional?

This is what I happen to think is our stroke professions major failing. They haven't kept up with the research. Without this there can never be a strategy. There are probably thousands of research possibilities that I have written about and I'm sure I've missed thousands more. Everyone seems to be sitting on their university knowledge and hoping that will get them through their career. CMEs are not the answer because they only are for the major topics. True stroke professionals would be all over me and pointing out exactly where I'm wrong. Yet no professional seems to have ever commented on my blog.
Seth Godin again;

Did you do the reading?

It's absurd to think of going to a book group meeting and opining about a book you didn't even read.
More rude: Going to a PhD seminar and participating in the discussion without reading the book first.
And of course, no one wants a surgeon operating on them if she hasn't read the latest journal article on this particular procedure.
It makes no sense to me to vote for a candidate who doesn't care enough to have read (and understood) the history of those that came before.
A first hurdle: Are you aware of what the reading (your reading) must include? What's on the list? The more professional your field, the more likely it is that people know what's on the list.
The reading isn't merely a book, of course. The reading is what we call it when you do the difficult work of learning to think with the best, to stay caught up, to understand.
The reading exposes you to the state of the art. The reading helps you follow a thought-through line of reasoning and agree, or even better, challenge it. The reading takes effort.
If you haven't done the reading, why expect to be treated as a professional?

Objective real-time motion analysis using wearable devices for post stroke rehabilitation

It takes a graduate student to think up these innovative ideas.

Committee Chair

Sartipi, Mina

Committee Member

Yang, Li; Liang, Yu; Ward, Mike


Dept. of Computer Science and Engineering


College of Engineering and Computer Science


University of Tennessee at Chattanooga

Place of Publication

Chattanooga (Tenn.)


With the growing population of the elderly, there is an increasing need for reliable, inexpensive, and quantifiable clinical measures. This thesis proposes mStroke, a practical, accurate, and mobile health system that remotely measures a stroke patient's proficiency in standard post-stroke therapy activities. The proposed system is delivered as an application (App) running on a hardware system consisting of two bluetooth low energy (BLE) modular sensor devices and an iPad. The system uses accelerometers, gyroscopes, and magnetometers to measure movement during three single-tasked clinical activities: the functional reach test, the NIHSS motor arm test, and the NIHSS motor leg test. The proposed system has been extensively tested using emulated and real data from physical therapy students. Key Words: Motion Analysis, Stroke, Functional Reach, NIHSS.


M. S.; A thesis submitted to the faculty of the University of Tennessee at Chattanooga in partial fulfillment of the requirements of the degree of Master of Science.




Motor ability -- Testing; Cerebrovascular disease -- Patients -- Rehabilitation; Human-computer interaction


Motion Analysis; Stroke; Functional Reach; NIHSS


Computer Sciences

Document Type

Masters theses


x, 46 leaves




Under copyright.


Intraventricular Infusion of a Low Fraction of Serum Enhances Neurogenesis and Improves Recovery in a Rodent Stroke Model

Is this interesting enough to be proposed for human clinical trials? I want to know whom in the world can answer that question and then follow thru with the research to prove it one way or another. But that won't occur because we have no stroke strategy or stroke leaders at all.
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A serum fraction (100K) was easily derived from serum.
100K/bFGF enhanced cell proliferation at SVZ area and infarcted brain.
100K/bFGF increased the number of MAP-2 cells at infarcted brain in MCAO rat.
100K/bFGF improved animals' motor coordination of MCAO rat.


Enhancing endogenous neurogenesis is a potential therapeutic strategy in stroke treatment. We have previously domonstrated that treatment with a fraction of serum with molecular weight of less than 100kDa (100K) combined with bFGF promoted neurogenesis of cultured stem and progenitor cells (NSPCs). In this study, we further evaluated the efficacy of intraventricular administration of 100K with bFGF (100K/bFGF) in a rat model of transient middle cerebral artery occlusion (MCAO). Rats administered 100K/bFGF on post-stroke day 1 exhibited a higher number of Ki67 and Nestin immunoreactive cells at the subventricular zone (SVZ) area and in the infarcted brain, indicating promotion of NSPCs proliferation. The 100K/bFGF treatment also predominantly increased the number of MAP-2 immunoreactive cells rather than GFAP immunoreactive cells at the SVZ area and in the infarcted regions, implying that 100K/bFGF dominated NSPCs differentiating into neurons rather than astrocytes. Importantly, treatment with 100K/bFGF significantly improved the animals' motor coordination. These findings demonstrated that treatment with a low serum fraction and bFGF benefited ischemic stroke likely through promotion of the proliferation and neuronal differentiation of endogenous NSPCs.

Saturday, November 21, 2015

Systemic Proteasome Inhibition Induces Sustained Post-stroke Neurological Recovery and Neuroprotection via Mechanisms Involving Reversal of Peripheral Immunosuppression and Preservation of Blood–Brain–Barrier Integrity

This sounds like something that needs further research into translating into a hyperacute stroke protocol. But it won't occur because we have no strategy and no person in charge of executing that strategy. So we will be screwed for another 50 years at least.
  • Thorsten R. Doeppner 
  • , Britta Kaltwasser
  • , Ulrike Kuckelkorn
  • , Petra Henkelein
  • , Eva Bretschneider
  • , Ertugrul Kilic
  • , Dirk M. Hermann
$39.95 / €34.95 / £29.95 *
* Final gross prices may vary according to local VAT.
Get Access


In view of its profound effect on cell survival and function, the modulation of the ubiquitin-proteasome-system has recently been shown to promote neurological recovery and brain remodeling after focal cerebral ischemia. Hitherto, local intracerebral delivery strategies were used, which can hardly be translated to human patients. We herein analyzed effects of systemic intraperitoneal delivery of the proteasome inhibitor BSc2118 on neurological recovery, brain injury, peripheral and cerebral immune responses, neurovascular integrity, as well as cerebral neurogenesis and angiogenesis in a mouse model of transient intraluminal middle cerebral artery occlusion. Systemic delivery of BSc2118 induced acute neuroprotection reflected by reduced infarct volume when delivered up to 9 h post-stroke. The latter was associated with reduced brain edema and stabilization of blood–brain–barrier integrity, albeit cerebral proteasome activity was only mildly reduced. Neuronal survival persisted in the post-acute stroke phase up to 28 days post-stroke and was associated with improved neurological recovery when the proteasome inhibitor was continuously delivered over 7 days. Systemic proteasome inhibition prevented stroke-induced acute leukocytosis in peripheral blood and reversed the subsequent immunosuppression, namely, the reduction of blood lymphocyte and granulocyte counts. On the contrary, post-ischemic brain inflammation, cerebral HIF-1α abundance, cell proliferation, neurogenesis, and angiogenesis were not influenced by the proteasome inhibitor. The modulation of peripheral immune responses might thus represent an attractive target for the clinical translation of proteasome inhibitors.

A reason persuasion is surprisingly difficult - stroke leaders?

Knowing how to do this in stroke is imperative. We have to somehow convince everyone in stroke leadership positions that they have no clue in how to solve anything in stroke.
Another great Seth Godin blog post.
Each of us understands that different people are swayed by different sorts of arguments, based on different ways of viewing the world. That seems sort of obvious. A toddler might want an orange juice because it's sweet, not because she's trying to avoid scurvy, which might be the argument that moves an intellectual but vitamin-starved sailor to take action.
So far, so good.
The difficult part is this: Even when people making an argument know this, they don't like making an argument that appeals to the other person's alternative worldview.
This is key. What is the worldview of stroke leaders that they don't see all the problems in stroke and just focus on press releases, prevention tidbits and F.A.S.T.?
Worth a full stop here. Even when people have an argument about a political action they want someone else to adopt, or a product they want them to buy, they hesitate to make that argument with empathy. Instead, they default to talking about why they believe it.

Impact of High-Fat Diet on Red Blood Cells May Cause Cardiovascular Disease

Which way is your doctor and hospital leaning for fat in diets? Do they have any dietary protocol at all?
Maybe you want to read this article which suggests that sugar is the problem;

The evidence for saturated fat and for sugar related to coronary heart disease

Impact of High-Fat Diet on Red Blood Cells May Cause Cardiovascular Disease 

University of Cincinnati researchers have discovered the negative impact a high fat diet has on red blood cells and how these cells, in turn, promote the development of cardiovascular disease. 

This is one of the first studies to demonstrate the effect of red blood cells on the disease and could also affect the way patients with other health conditions, like cancer, who are prone to developing cardiovascular issues, are diagnosed and treated. It will be published in the Nov. 17 edition of the journal Circulation with an accompanying editorial. 

"Obesity caused by chronic consumption of a high-calorie, high-fat diet is a worldwide epidemic, representing one of the greatest threats to global health,” says principal investigator Vladimir Bogdanov, PhD, associate professor and director of the Hemostasis Research Program within the Division of Hematology Oncology at the UC College of Medicine and member of the Cincinnati Cancer Center and UC Cancer Institute. "White blood cells play a key role in fueling adipose tissue (fat) inflammation and insulin resistance in obesity and also promote the clogging of arteries, or atherosclerosis, setting the stage for heart attack and stroke. While these outcomes linked with a high fat diet and fat in the blood on white blood cells have been shown in animal models and humans, the impact of high fat diets on other bone marrow-derived cells, like red blood cells, is not well defined.

"Evidence is emerging that red blood cells play an important regulatory role in the development of atherosclerosis, binding pro-inflammatory proteins that cause dysfunction in the inner lining of the blood vessel wall—the endothelium. We explored how a high fat-diet causes red blood cell dysfunction in this study.”

Bogdanov and his team fed a 60 percent high-fat diet to a group of animal models for 12 weeks and saw an increased amount of key proteins that stimulate white blood cells bound to red blood cells. These white blood cells, also known as macrophages, are a type of white blood cell that "eats” cellular debris, foreign substances, microbes, cancer cells and anything else that does not have the types of proteins specific to the surface of healthy body cells on its surface. They also play a crucial role in atherosclerosis.

"In red blood cells from animal models fed a high-fat diet, there was an increase in cholesterol found in the cell membrane and phosphatidylserine levels, promoting inflammatory reactions. Phosphatidylserine is a phospholipid membrane component which plays a key role in the cycle of cells,” Bogdanov says. "When red blood cells from the animals being fed the high-fat diet were injected into a control group, eating a normal diet, there was a three-fold increase in their spleens’ uptake of red blood cells. The spleen is involved in the removal of blood cells, as well as systemic inflammation.

"All of these findings show that the dysfunction of red blood cells, corresponding with dysfunction of the lining of blood vessels, occurs very early in diet-induced obesity and may play a part in the formation of atherosclerosis. Diets high in saturated fat have long been associated with endothelial dysfunction, the precursor to atherosclerosis, but to our knowledge, the effects of high-fat diet on red blood cells have not been rigorously examined.”

He adds that in humans, high cholesterol is associated with alterations in red blood cells which are improved by treatment with statins, but the majority of obese humans do not have severe high cholesterol as was the case with the animal models in the study. 

Bogdanov stresses that this project would have never been successful were it not for a close collaboration between his lab and that of Professor Neal Weintraub, MD, from the Vascular Biology Center at the Medical College of Georgia, Georgia Regents University (GRU). Weintraub, who is a co-principal investigator and a former UC faculty member, is working on expanding the team’s findings in animal models to human disease. His team has recently conducted a study which demonstrated that a single high-fat meal produces harmful effects on red blood cells in humans. Bogdanov adds that these findings may also help patients with cancer who are frequently prone to thrombosis (blood clots).

"This study was funded using start-up funds I received from the university when I came here, which also helped me collaborate with other labs, like that of Dr. Weintraub’s, Dr. (Xiaoyang) Qi’s in my own division, throughout the medical campus and elsewhere in the country and abroad, to create an academically balanced study touching on aspects of both cardiovascular disease and cancer. These types of packages are vital for making progress on innovative research that may not otherwise be feasible.”

Scientists look to heart disease and strokes for clues to treating Alzheimer's

So what is the link between stroke and dementia/Alzheimers? Does your doctor know anything? Have a protocol to prevent your descent into dementia? Doing ANYTHING AT ALL?
Your 33% dementia chance post-stroke from an Australian study?
Then this study came out and seems to have a range from 17-66%.
A 20% chance in this research.
A growing body of research suggests that the most common cause of dementia in older people is a mix of vascular and Alzheimer's-related brain abnormalities, and that approximately half of people who die with Alzheimer's also have evidence of strokes in their brains. Furthermore, when strokes and hallmark Alzheimer's plaques and tangles are combined, it increases a person's likelihood of experiencing dementia. Stroke, or as it is known more generally as cerebrovascular disease, occurs with aging and is made worse by conditions like smoking, hypertension or diabetes.
Recommendations by a group of scientists to bolster research on how Alzheimer's and vascular conditions progress together and influence each other are available online today, in advance of publication, by Alzheimer's & Dementia: The Journal of the Alzheimer's Association. The authors hope this research agenda, if executed, will uncover new clues for effectively treating or preventing .
"We are encouraged by the potential for new treatment strategies for dementia to arise from studying the crossover of vascular factors with the progression of Alzheimer's," says Heather M. Snyder, Ph.D., director of medical and scientific operations for the Alzheimer's Association, and first author of the new article. "In terms of next steps, we need to develop the research tools and collaborations necessary to further scientific investigation in this promising area of study."
Cerebrovascular disease can be prevented with a variety of drug and lifestyle interventions; however, this has not yet been established for dementia. Snyder says, "Whether improved control of vascular risk factors can be translated to decreased dementia risk is not known, but results from a number of studies suggest that it is possible, and this untapped potential definitely deserves greater research attention."
In December 2013, the Alzheimer's Association, with scientific input from the National Institutes of Health's National Institute of Neurological Disorders and Stroke (NINDS) and National Heart, Lung and Blood Institute (NHLBI), convened a group of scientific experts to discuss the scientific findings to date and gaps in research on vascular contributions in Alzheimer's and related forms of dementia. The newly-published article summarizes the meeting and discussions, including an outline of next steps.
"Blood vessels that deliver nutrients to the and carry away waste are vital for normal cognitive function," says co-author Roderick Corriveau, Ph.D., the NINDS program director who oversees dementia research. "Understanding vascular contributions to cognitive impairment and dementia, including changes due to , heart disease and diabetes, are critically important to guide the development of preventions and treatments for dementia."
"Inadequate blood flow can damage and eventually kill cells anywhere in the body," says Donna M. Wilcock, Ph.D., a neurovascular researcher who is an assistant professor in the Department of Physiology at the University of Kentucky College of Medicine in Lexington and a co-author of the paper. "Since the brain has one of the body's richest networks of blood vessels, it is especially vulnerable. Considering this and demonstrated success in reducing risk for heart disease, stroke and other vascular-related diseases through healthy lifestyle modifications and use of medications, it only makes sense to increase our understanding of the role vascular factors play in Alzheimer's and dementia."
The authors of the article recommend filling gaps in several key areas of research, including:
  • The relationship between diabetes and insulin resistance and risk of vascular disease, Alzheimer's and related dementia.
  • Genetic factors that may influence vascular processes and other changes in the brain.
  • Impact of immune system response on blood flow in the brain in the progression of Alzheimer's disease.
  • The role of fat breakdown in the brain in the removal of amyloid build-up that leads to the hallmark brain plaques in Alzheimer's disease.
  • Controlling the impact of vascular risk factors on memory and thinking abilities.
The authors also conclude that biological markers, which are used to detect and measure disease progression, of key vascular processes related to impairment of brain function, memory and thinking abilities are needed to move this research further and faster.
"Having the methods to detect early signs of vascular-related brain injury or disease with the greatest impact on Alzheimer's and dementia would greatly enhance our efforts to develop effective therapies," says David Knopman, M.D., professor of neurology at the Mayo Clinic College of Medicine in Rochester, MN, and a co-author of the paper. "Especially needed are tools that are highly accurate and do not require invasive procedures to collect and measure." Dr. Knopman is vice chair of the Alzheimer's Association Medical and Scientific Advisory Council.
Among the biological markers the authors say are necessary are:
  • Ability to detect amyloid in blood vessels in the brain.
  • Imaging technology that can detect changes from dying brain tissue.
  • Indicators of risk for Alzheimer's in pre-diabetic individuals.
  • Improved methods for measuring the impact of blood flow in the brain on memory and thinking abilities.
"Future investment for these areas of scientific discovery will be essential to galvanize the scientific community and provide forums of communication between the dementia and vascular fields," the authors state in the paper.
As a further next step, research sessions and scientific presentations focusing on the relationship between vascular factors, Alzheimer's disease and related dementias are being planned for upcoming major scientific and medical conferences—including meetings hosted or sponsored by the Alzheimer's Association, the American Heart Association, and the National Institutes of Health.

Could Old Gout Drug Offer New CV Benefits?

We'll never know at least as long as our fucking failures of stroke associations don't have a strategy to find solutions to all the problems in stroke.  You'll want to read my 3 posts on gout to see if you'd want gout to have it for the benefits.
The elevated risk of cardiovascular events among patients with gout declined in those who used colchicine, an observational study found.
The incidence rate ratios among colchicine users compared with non-users were 0.52 (95% CI 0.29-0.92) for myocardial infarction, 0.34 (95% CI 0.14-0.71) for stroke, and 0.79 (95% CI 0.24-2.39) for transient ischemic attack, according to Daniel H. Solomon, MD, and colleagues from Brigham and Women's Hospital in Boston.
After adjustment for all covariates including age, sex, race, history of CV disease, diabetes, and hypertension, and the use of medications such as statins and aspirin, the risk of a composite CV endpoint that included all these events was 49% lower among gout patients who took colchicine (HR 0.51, 95% CI 0.30-0.88, P=0.016), the researchers reported online in Annals of the Rheumatic Diseases.
"While we are unable to confirm a causal link in a non-randomized observational study, this study provides justification for a randomized controlled trial of colchicine to reduce CV risk among patients with gout," Solomon and colleagues stated.
Because atherosclerosis is strongly associated with inflammation, there are current efforts to explore the possibility of using immunomodulatory medications including colchicine, methotrexate, and canakinumab (Ilaris) for prevention.
Colchicine "downregulates inflammation through blocking microtubule spindle formation, disrupting inflammasome function, inhibiting cytokine production, and hindering neutrophil chemotaxis," the researchers explained.
Previous studies have suggested that the drug -- used in gout for hundreds of years -- was beneficial for secondary CV prevention in the general population, but little is known about its CV prevention effects in gout patients themselves.
Therefore, the researchers analyzed data from the Brigham and Women's Hospital electronic medical records and the linked Medicare databases for the years 2006 to 2011.
They identified 501 patients with gout who had a first prescription for colchicine during that time, matching them by age, gender, and index date with gout patients without colchicine prescriptions.
Average age was 73, and two-thirds of the study participants were men. The cases and controls were similar in history of heart failure, CV disease, and chronic kidney disease, but cases had more hypertension (77% versus 28%, P<0.0001), had higher body mass index, and more commonly used allopurinol, nonsteroidal anti-inflammatory drugs, and especially statins (50% versus 16%, P<0.0001). Median follow-up was 1.3 years.
While the rates of myocardial infarction, stroke, and transient ischemic attack were lower in the colchicine group, the rates of revascularization procedures were similar. For coronary artery bypass grafts, the incidence rate ratio was 3.11 (95% CI 0.71-18.62), and for percutaneous coronary intervention the ratio was 1.03 (95% CI 0.59-1.78).
In an additional analysis using all-cause mortality as the outcome, colchicine users had a lower risk, with a hazard ratio of 0.27 (95% CI 0.17-0.43, P<0.0001).
Colchicine typically is not used for extended periods, but rather is given for the acute attack or at the initiation of urate-lowering therapy, but some patients with frequent flares have used it long term.
"These results, along with those from prior studies, suggest that long-term colchicine may provide CV risk protection among patients with gout with and without known cardiovascular disease, a group known to experience a 30% to 60% increased risk of CV events," Solomon and colleagues observed.
However, they advised that their findings should be interpreted with caution, noting that prescriptions for colchicine may have been more commonly given to patients willing to take medications, or that providers may have hesitated to prescribe the drug to the sickest patients. There also could have been residual confounding.
"Results from this study may be considered hypothesis-generating for a formal test of whether colchicine reduces CV risk in the setting of a randomized controlled trial," they concluded.
If the drug does succeed in decreasing CV risk in a formal study, it is likely that the effects derive from colchicine's immunomodulatory effects, as it does not lower uric acid, the investigators noted.
The study was supported by the National Institutes of Health.
The authors reported financial relationships with Lilly, Pfizer, Amgen, and AstraZeneca.
  • Reviewed by Robert Jasmer, MD Associate Clinical Professor of Medicine, University of California, San Francisco and Dorothy Caputo, MA, BSN, RN, Nurse Planner
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probiotics and tryptophan may slow down social cognitive decline in aging.

Would this help us post-stroke? Let your doctor know that you want to know the results when they are released. Charge him/her $1000 for training if you have to notify them them that the results are out. Your doctor should have a system in place that notifies them when relevant stroke research comes out. And that shouldn't be me, if they are relying on me and you to keep up to date that is a sign of pure incompetence.
A JPI "A Healthy Diet for A Healthy Life" / Joint Transnational grant (1.000.000 Euro) has been awarded to Dutch, German and Spanish interdisciplinary scientists to investigate whether the administration of probiotics and tryptophan may slow down social cognitive decline in aging.

Within twenty years Europe will face a situation where the largest population cohort will be those over the age of 65. The aim of the awarded research program is to understand how social cognition, a crucial factor for successful aging and vitality, can be preserved and promoted in old age. This project will be jointly carried out by Peter Kirsch (Central Institute of Mental Health, Germany), Lorenza Colzato (Leiden University, The Netherlands), Martin Reuter (University of Bonn, Germany) and Ana Rodríguez Moratinos (University of Extremadura, Spain). Using a multidisciplinary and translational approach, this project will be the first to examine how probiotics and tryptophan can enhance social and affective cognition in aging. Epigenetics (changes in gene expression triggered by the environment) will be used to study and understand the mechanisms underlying the interactions between brain, nutritional intervention, and social behavior. If successful, this approach would provide an important step towards developing food programs that are tailored to individual needs. The proposed research is the first to combine genetics, epigenetics and nutritional intervention studies from a social cognitive neuroscience perspective.

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.



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.


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.


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).


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.


URL: Unique identifier: NCT00989716.

VIB research presents new insights in the search for treatments for neurological diseases

What is your doctor going to do with this information to help your recovery? You probably need to train your doctor in this.
A team of researchers led by professor Patrik Verstreken (VIB/KU Leuven) has exposed the fine details of a mechanism that provides more insight in the communication between neurons. The research has clarified how damaged synapses – the connection points between neurons – are repaired to keep communication between neurons at an optimal level. Disturbances in these mechanisms are believed to play a role in the development of neurodegenerative diseases, such as dementia, ALS or Parkinson’s disease. The results have been published in leading neuroscience journal ‘Neuron’.

Our brains are made up of billions and billions of nerve cells or neurons that gather and transmit signals via so-called synapses. These synaptic connections between neurons transmit ‘electrical firings’ via chemical messengers (neurotransmitters). Synapses thus contribute to numerous bodily functions, including speech, thoughts and voluntary actions.

Disruption of synaptic transmission
Prof. Patrik Verstreken (VIB/KU Leuven): “Synapses are the active part of neurons, and this activity causes some damage in the long term. Fortunately, synapses are capable of breaking down and ‘recycle’ damaged cellular components. Our study has largely revealed the process behind this. It is quite a significant discovery, especially when you consider that many neurological diseases, such as Parkinson’s, ALS or dementia, but also speech or motion disorders for instance, are caused by the disruption of synaptic transmission.”

Cellular debris
Prior research revealed that several different proteins play a role in neuronal communication. However, these same proteins can also cause disruptions. This happens, for instance, when proteins split, causing their particles to stick together and clump. This ‘cellular debris’ then disrupts synaptic transmissions and may contribute to the development of neurodegenerative diseases.

The importance of ‘microautophagy’
Prof. Patrik Verstreken (VIB/KU Leuven): “We studied the proteins involved, both in vitro and in vivo and, in doing so, exposed a mechanism called ‘synaptic microautophagy’. This mechanism helps ‘clean up’ cellular debris at the synapse, by engulfing the debris in a membrane and then removing it, for instance. It ensures that the cellular debris is isolated from the rest of the synapse. We found that synaptic communication slows down when microautophagic activity is reduced (i.e. when the cellular debris is not broken down) and that it speeds up when microautophagic activity increases (when more cellular debris is broken down). This discovery therefore represents an important advance in the search for treatments for neurodegenerative diseases, such as Alzheimer’s – which are caused by clumped together cellular debris.”

Pathways for further research
The study conducted by prof. Verstreken and his team once again emphasizes the need for ongoing research into neuronal communication. Such research could examine substances that may counteract the progress of neurodegeneration in neurons. This would aid the search for potential drug treatments for neurological diseases, such as Alzheimer’s.

The Meeting of the Minds Dementia Conference

Look what a good patient association can do. I don't think our fucking failures of stroke associations even want to talk to survivors. Stroke survivors are damned easy to find, they're all over facebook and self created stroke forums. Yeah, stroke survivors can be hard to talk to, like those with aphasia and those that still have high cognitive abilities, some with both.  They would get an earful and our stroke associations seem to just put out press releases, not do any actual work.
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The Meeting of the Minds Dementia Conference is the premier dementia conference for people with Mild Cognitive Impairment (MCI) or early dementia, families, friends and professionals. The conference is a collaboration between the Alzheimer's Association and Mayo Clinic, who work together to create a day filled with dementia information, support and resources. Every year national, regional and local presenters come together to ensure an innovative and insightful conference for the 1,300 participants and over 70 sponsors and exhibits. 15 Meeting of the Minds Gallery PhotoPhoto: Scott Nelson
Saturday, March 19, 2016  
7:30 a.m. - 4:30 p.m.
General Conference registration will open on January 4, 2016 at 9 a.m. 

Saint Paul RiverCentre
175 West Kellogg Boulevard
Saint Paul, MN 55102
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Registration will open at 9 a.m. and end at 5 p.m. (Central Time) on the respective days.
EARLY BIRD(1/4-2/5) STANDARD(2/6-3/14)

$80  $100


Mary Mittelman, D.P.H.
Dr. Mary Mittelman is Research Professor of Psychiatry and Rehabilitative Medicine at NYU School of Medicine. She is an epidemiologist who has been developing and evaluating psychosocial interventions for people with cognitive impairment and their family members for nearly three decades. For more than 20 years, Dr. Mittelman was Principal Investigator of the National Institute of Health funded study of the NYU Caregiver Intervention (NYUCI), which has been widely published and recognized. With her colleagues, she developed online training for social service professionals as well as a telehealth version of the NYUCI. In 2004, Dr. Mittelman was the recipient of the Alzheimer’s Association Zenith Fellows Award for her research on the effectiveness of counseling for couples impacted by dementia. In the past decade, Dr. Mittelman has been evaluating and developing interventions that include the people with dementia with their caregiver, and founded The Unforgettables, a chorus for people with dementia with their family members.

Donald Warne, MD, MPH
Donald Warne, MD, MPH is Professor and Chair of the Department of Public Health in the College of Health Professions at North Dakota State University, and he is the Senior Policy Advisor to the Great Plains Tribal Chairmen’s Health Board. Dr. Warne is a member of the Oglala Lakota tribe from Pine Ridge, SD and comes from a long line of traditional healers and medicine men. He received his MD from Stanford University School of Medicine and his MPH from Harvard School of Public Health.

Professional activities include:
  • Member, National Board of Directors, American Cancer Society 
  • Member, Minority Affairs Section and Association of American Indian Physicians Representative to the American Medical Association 
  • Member, Advisory Committee on Rural Health and Human Services, US Department of Health and Human Services
  • Member, Advisory Committee on Breast Cancer in Young Women, Centers for Disease Control and Prevention 
  • Member, National Institutional Review Board, Indian Health Service 

For more information about the Meeting of the Minds Dementia Conference 2016, contact Deborah Richman, Vice President, Education & Outreach:

By phone: 952.857.0551 
By email: 

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