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:

Friday, August 22, 2014

At Penn State, telemedicine boosts stroke care to rural patients

This may be the best we can do under the current circumstances. But the status quo is f*cking appalling. tPA efficacy is only 12% and does nothing to stop the neuronal cascade of death. But our stroke medical world will not open their eyes and acknowledge that everything in stroke is a f*cking failure.
Absolutely everything in stroke is a failure and has been for 30 years.
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.
2. Only 10% get to almost full recovery.
3. 12% tPA efficacy
4. Nothing being done to stop the neuronal cascade of death during the first week.
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.

But here is the latest back patting;

Not only cardiovascular, but also coordinative exercise increases hippocampal volume in older adults

You will need to ask your doctor for what exactly is a coordination exercise and the stroke protocol that goes with it.
  • 1Jacobs Center on Lifelong Learning and Institutional Development, Jacobs University Bremen, Bremen, Germany
  • 2AgeAct Research Center, Jacobs University Bremen, Bremen, Germany
Cardiovascular activity has been shown to be positively associated with gray and white matter volume of, amongst others, frontal and temporal brain regions in older adults. This is particularly true for the hippocampus, a brain structure that plays an important role in learning and memory, and whose decline has been related to the development of Alzheimer’s disease. In the current study, we were interested in whether not only cardiovascular activity but also other types of physical activity, i.e., coordination training, were also positively associated with the volume of the hippocampus in older adults. For this purpose we first collected cross-sectional data on “metabolic fitness” (cardiovascular fitness and muscular strength) and “motor fitness” (e.g., balance, movement speed, fine coordination). Second, we performed a 12-month randomized controlled trial. Results revealed that motor fitness but not metabolic fitness was associated with hippocampal volume. After the 12-month intervention period, both, cardiovascular and coordination training led to increases in hippocampal volume. Our findings suggest that a high motor fitness level as well as different types of physical activity were beneficial to diminish age-related hippocampal volume shrinkage or even increase hippocampal volume.


It has repeatedly been shown that physical activity is positively related to brain structure and function (see Kramer et al., 2006; Hillman et al., 2008; Park and Reuter-Lorenz, 2009) as well as cognitive performance (for a review see Etnier et al., 2006) and that it might reduce the risk of developing dementia (Sumic et al., 2007; Erickson et al., 2012). Particularly the hippocampal formation has been in the focus of these studies investigating the positive effect of physical activity on brain volume because this brain structure is thought to be significantly involved in diseases related to memory impairment like, e.g., Alzheimer’s disease (Driscoll et al., 2003; Barnes et al., 2009). Whereas positive correlations between cardiovascular activity and hippocampal volume have been shown, it is unknown whether this applies to other types of physical activity like, e.g., coordination training, as well. With this paper we aim to extend the knowledge about the effects of different physical activity interventions in older adults and its potential to diminish the decline in hippocampal volume during the aging process.

The Hippocampus and its Shrinkage Across the Adult Lifespan

The hippocampal formation as part of the limbic system is located in the medial temporal lobe. It is highly involved in processes of episodic memory formation (Tulving and Markowitsch, 1998; Van Petten, 2004) and spatial navigation (O’Keefe, 1990; Maguire et al., 2000). Both cognitive dimensions are especially vulnerable to performance loss in late adulthood (cf. Hedden and Gabrieli, 2004). Recently, the hippocampus has also been associated with motor sequence consolidation (Albouy et al., 2008). Over the adult lifespan, on average, hippocampal volume shrinks about 0.86% per year, but this development is highly non-linear (Raz et al., 2004b). Whereas for adults below the age of 50 annual hippocampal volume reductions of only 0.51% were observed, adults above the age of 50 revealed a much steeper annual volume decline of 1.18% (Raz et al., 2004b). These volume reductions are mainly attributed to reductions in the neuropil part of the brain structure and – to a smaller extend – to cell body shrinkage and changes in vascularization (Thomas et al., 2012).

Current statistics indicate that there are more than 7 million people in the United States who have survived a stroke or brain attack and are living with the after-effects.

The National Stroke Association posts these statistics. But reading the rest of the page there is absolutely nothing on there that will help any of those survivors. They need to remove Stroke from their title, they have absolutely nothing to do with stroke survivors.
So they know nothing about about how to engage neuroplasticity. No references to Pedro Bach-y-Rita. Nothing on

The man with the missing brain

Nothing on neurogenesis.
What the hell good does it do if you state there is a problem but offer no solutions?
And I know the mantra from them is

'This question falls under our organizational guidelines as a medical inquiry and we defer to the medical community to respond. '


TeleStroke units improve stroke care in underserved areas

This may be the best we can do under the current circumstances. But the status quo is f*cking appalling. tPA efficacy is only 12% and does nothing to stop the neuronal cascade of death.
But our stroke medical world will not open their eyes and acknowledge that everything in stroke is a f*cking failure.
Absolutely everything in stroke is a failure and has been for 30 years.
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.
2. Only 10% get to almost full recovery.
3. 12% tPA efficacy
4. Nothing being done to stop the neuronal cascade of death during the first week.
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.

But here is the latest back patting;

Thursday, August 21, 2014

Your Brain’s Future: The Good And Bad News

A blog post from The Best Brain Possible
You need to read the quotes from Dr. Michael Merzenich 
 My ideas here: Dementia prevention 19 ways 

Mayo Clinic first in Florida to receive national comprehensive stroke center certification

Ok, maybe you are good at processes but that is meaningless if the results are not successful. The results to look at are 30 day deaths, 100% recovery and complete reversal of stroke effects using tPA. If you can't tout these then you are not a very good stroke center.
 I personally believe the Joint Commissions  stuff on stroke is worthless.
You can check out Joint Commission standards here:
I saw absolutely nothing about what should be done the first week or anything about measuring 30-day deaths and 100% recovery or tPA efficacy. 

How Stress Promotes Atherosclerosis

You will need to demand that your doctor remove all the stressors from your hospital environment.
1. Poor sleep
2. No objective diagnosis of damage.
3. No path to 100% recovery.
4. Nocebo comments about no further recovery/plateau.
5. Worries about cognitive decline with no stroke protocol to fix that.
6. Fatigue.
7. Spasticity which your doctor has no idea how to cure.
Atherosclerosis is an inflammatory disease characterized by the “hardening” of the arteries. This is caused by the accumulation of deposits mainly composed of cell debris, fats, cholesterol, calcium, on the inner walls of arteries leading to vessels’ narrowing and decreased blood flow. These deposits are called plaques and they also contain platelets and immune cells (leukocytes), in particular inflammatory monocytes and macrophages. Enzymes produced by the immune cells can partially degrade the plaques causing their disruption and cause formation of blood clots that will occlude the vessels and block oxygen supply to different organs and tissues. If a clot occurs in vessels of the heart or the brain, it will elicit a heart attack or a stroke respectively.
Link between stress and atherosclerosis
There is evidence that chronic stress increases the risk of atherosclerosis, but no mechanism linking the two phenomena has been demonstrated so far. Since stressful emotional states can affect the function of the immune system, Heidt and colleagues of the Massachusetts General Hospital hypothesized that stress increases the activity of inflammatory cells in the plaques facilitating their rupture, as you can read in their recently published article.
To test this possibility the scientists measured the effects of various forms of stress (including isolation, damp bedding, overnight illumination) on the number of leukocytes in mice. They found that compared to the controls the stressed animals had significantly more circulating immune cells. This was the result of increased division of the hematopoietic stem cells (HSCs), which are the immature precursors of the immune cells, and subsequent increased production of leukocyte progenitors in their bone marrow.

More at link.

Coenzyme Q10 Increases Cholesterol Efflux and Inhibits Atherosclerosis Through MicroRNAs

What does your doctor have to say about this?
Can coenzyme Q10 reduce the risk of side effects from statins?

Or is this  atherosclerosis inhibition a better reason for it?
  1. Kasey C. Vickers
+ Author Affiliations
  1. From the Department of Medicine, Vanderbilt University School of Medicine, Nashville, TN.
  1. Correspondence to Kasey C. Vickers, PhD, Department of Medicine, Vanderbilt University School of Medicine, 2220 Pierce Ave 312B PRB, Nashville, TN 37232. E-mail
Key Words:
Atherosclerosis is a progressive inflammatory disease of the artery wall and the underlying basis for cardiovascular disease (CVD), which accounts for ≈32% of all deaths in the United States and is the leading cause of mortality in the world.1 Atherosclerosis is classically defined by the accumulation of lipid and cholesterol deposits within the subendothelial space in the artery wall which leads to chronic inflammation and proinflammatory, cholesterol-laden macrophages which differentiate into resident foam cells in the lesion, ultimately forming an acellular necrotic core.2 To date, the statin drug class has been overwhelmingly successful at reducing circulating total cholesterol levels, namely low-density lipoproteins cholesterol, the number one risk factor for CVD. Although pharmacological intervention with statins has dramatically reduced the number of cardiovascular events, many patients do not tolerate statins and a substantial disease burden remains even in patients who are on statins. Therefore, a great need remains to identify new drug targets and novel approaches to prevent and treat atherosclerosis and CVD. One strategy that has been extensively studied, but remains central to atherosclerosis reduction, is identifying new ways to increase the removal of excess cholesterol from peripheral cells and lesions through the reverse cholesterol transport (RCT) pathway. Briefly, the RCT pathway involves the transport of cholesterol from peripheral tissues (ie, foam cells within atherosclerotic lesions) to the liver by high-density lipoproteins (HDL), where cholesterol is excreted from the body as bile.3 This pathway is mediated by a number of lipid and cholesterol transporters, including the widely …

From Hairballs to an Understanding of Transendothelial Migration of Monocytes in Atherosclerosis

If hairballs are listed in the full article I'm not paying for it. But ask your doctor for the explanation.
  1. Aldons J. Lusis
+ Author Affiliations
  1. From the Departments of Medicine (M.C., A.J.L.), Microbiology, Immunology and Molecular Genetics, and Human Genetics (A.J.L.), University of California, Los Angeles.
  1. Correspondence to Aldons J. Lusis, PhD, Division of Cardiology, Department of Medicine, A2-237 CHS, University of California, Los Angeles, Los Angeles, CA 90095. E-mail
Key Words:
In the current issue of ATVB, Shang et al provide compelling evidence for the involvement of LIM domain binding 2 (LDB2) in the transendothelial migration of monocytes in atherosclerosis.1 The article is also of interest because of the systems analyses that led to its identification as a strong candidate.
See accompanying article on page 2068
LDB2 was identified earlier as a key driver of atherosclerosis based on studies of gene expression profiles of tissues obtained from patients.2 Using samples from the Stockholm Atherosclerosis Gene Expression (STAGE) study, the authors profiled gene expression of 5 atherosclerosis-relevant tissues from 114 patients undergoing coronary artery bypass grafting. The tissues collected were distal internal mammary artery, wall of the ascending aorta at the aortic root, anterior hepatic edge, skeletal muscle, and visceral fat. A total of 278 gene expression profiles were used in a coupled 2-way clustering analysis3 to identify 60 gene subnetworks in these tissues. Two of the gene clusters, one in atherosclerotic arterial wall (49 genes) and the other in visceral fat (59 genes), segregated the patients according to the extent of atherosclerosis as measured by quantitative coronary angiography. The authors further validated their findings using expression data obtained from carotid lesions isolated from patients undergoing carotid stenosis surgery. Clustering of data identified 8 gene subnetworks in carotid lesions, one of which segregated the patients according to the extent of atherosclerosis as measured by ultrasound-measured intima-media thickness. This cluster significantly overlapped with the 2 previously identified clusters from …

Facilitation of corticospinal excitability by virtual reality exercise following anodal transcranial direct current stimulation in healthy volunteers and subacute stroke subjects

Someday in the far distant future there will be a written protocol for walking recovery. If YOU want it sooner than that YOU will need to demand your therapist initiate a translational clinical research trial on how best to get stroke patients walking.  This is not going to occur without YOU pushing it from the bottom. And if your hospital does not have research projects as goals for all therapists and doctors then you have a hospital that should not be used. Screaming would probably help.
Pay it forward people or future survivors will be screwed even worse than you were.
Yeun Joon Kim, Jeonghun Ku, Sangwoo Cho, Hyun Jung Kim, Yun Kyung Cho, Teo Lim and Youn Joo Kang
For all author emails, please log on.
Journal of NeuroEngineering and Rehabilitation 2014, 11:124  doi:10.1186/1743-0003-11-124
Published: 18 August 2014

Abstract (provisional)


There is growing evidence that the combination of non-invasive brain stimulation and motor skill training is an effective new treatment option in neurorehabilitation. We investigated the beneficial effects of the application of transcranial direct current stimulation (tDCS) combined with virtual reality (VR) motor training.


In total, 15 healthy, right-handed volunteers and 15 patients with stroke in the subacute stage participated. Four different conditions (A: active wrist exercise, B: VR wrist exercise, C: VR wrist exercise following anodal tDCS (1 mV, 20 min) on the left (healthy volunteer) or affected (stroke patient) primary motor cortex, and D: anodal tDCS without exercise) were provided in random order on separate days. We compared during and post-exercise corticospinal excitability under different conditions in healthy volunteers (A, B, C, D) and stroke patients (B, C, D) by measuring the changes in amplitudes of motor evoked potentials in the extensor carpi radialis muscle, elicited with single-pulse transcranial magnetic stimulation. For statistical analyses, a linear mixed model for a repeated-measures covariance pattern model with unstructured covariance within groups (healthy or stroke groups) was used.


The VR wrist exercise (B) facilitated post-exercise corticospinal excitability more than the active wrist exercise (A) or anodal tDCS without exercise (D) in healthy volunteers. Moreover, the post-exercise corticospinal facilitation after tDCS and VR exercise (C) was greater and was sustained for 20 min after exercise versus the other conditions in healthy volunteers (A, B, D) and in subacute stroke patients (B, D).


The combined effect of VR motor training following tDCS was synergistic and short-term corticospinal facilitation was superior to the application of VR training, active motor training, or tDCS without exercise condition. These results support the concept of combining brain stimulation with VR motor training to promote recovery after a stroke.

The complete article is available as a provisional PDF. The fully formatted PDF and HTML versions are in production.

Scientists Discover Brain Area Responsible for Exercise Motivation

So your doctor will need to check this area for damage to see if you even have the motivation to exercise. And then have a stroke protocol to correct such damage and restore your motivation.
Scientists at Seattle Children’s Research Institute have discovered an area of the brain that could control a person’s motivation to exercise and participate in other rewarding activities – potentially leading to improved treatments for depression.
Dr. Eric Turner, a principal investigator in Seattle Children’s Research Institute’s Center for Integrative Brain Research, together with lead author Dr. Yun-Wei (Toni) Hsu, have discovered that a tiny region of the brain – the dorsal medial habenula– controls the desire to exercise in mice. The structure of the habenula is similar in humans and rodents and these basic functions in mood regulation and motivation are likely to be the same across species.  
Exercise is one of the most effective non-pharmacological therapies for depression. Determining that such a specific area of the brain may be responsible for motivation to exercise could help researchers develop more targeted, effective treatments for depression. 
“Changes in physical activity and the inability to enjoy rewarding or pleasurable experiences are two hallmarks of major depression,” Turner said. “But the brain pathways responsible for exercise motivation have not been well understood. Now, we can seek ways to manipulate activity within this specific area of the brain without impacting the rest of the brain’s activity.” 
Turner’s study, titled “Role of the Dorsal Medial Habenula in the Regulation of Voluntary Activity, Motor Function, Hedonic State, and Primary Reinforcement,” was published by the Journal of Neuroscience and funded by the National Institute of Mental Health and National Institute on Drug Abuse. The study used mouse models that were genetically engineered to block signals from the dorsal medial habenula. In the first part of the study, Turner’s team collaborated with Dr. Horacio de la Iglesia, a professor in University of Washington’s Department of Biology, to show that compared to typical mice, who love to run in their exercise wheels, the genetically engineered mice were lethargic and ran far less. Turner’s genetically engineered mice also lost their preference for sweetened drinking water. 
“Without a functioning dorsal medial habenula, the mice became couch potatoes,” Turner said. “They were physically capable of running but appeared unmotivated to do it.” 
In a second group of mice, Turner’s team activated the dorsal medial habenula using optogenetics– a precise laser technology developed in collaboration with the Allen Institute for Brain Science. The mice could “choose” to activate this area of the brain by turning one of two response wheels with their paws. The mice strongly preferred turning the wheel that stimulated the dorsal medial habenula, demonstrating that this area of the brain is tied to rewarding behavior.  
Past studies have attributed many different functions to the habenula, but technology was not advanced enough to determine roles of the various subsections of this area of the brain, including the dorsal medial habenula. 
“Traditional methods of stimulation could not isolate this part of the brain,” Turner said. “But cutting-edge technology at Seattle Children’s Research Institute makes discoveries like this possible.” 
As a professor in the University of Washington Department of Psychiatry and Behavioral Sciences, Turner treats depression and hopes this research will make a difference in the lives of future patients. 
“Working in mental health can be frustrating,” Turner said. “We have not made a lot of progress in developing new treatments. I hope the more we can learn about how the brain functions the more we can help people with all kinds of mental illness.”

Efficacy of a newly designed trunk orthosis with joints providing resistive force in adults with post-stroke hemiparesis

I can't even visualize what this would look like.
  1. Junji Katsuhira1
  2. Nodoka Miura1
  3. Tadashi Yasui2
  4. Takane Mitomi3
  5. Sumiko Yamamoto1
  1. 1Graduate school of International University of Health and Welfare, Tokyo, Japan
  2. 2Kawamura-Gishi Company, Ltd., Daito, Japan
  3. 3GK Dynamics, Tokyo, Japan
  1. Junji Katsuhira, International University of Health and Welfare, 1-2-25 Shiroyama, Odawara 250-8588, Japan. Email:


Background: Few studies have examined the efficacy of trunk orthoses that support the upper trunk and a paretic limb in stroke patients. To improve stability and alignment of the trunk and pelvis in hemiparetic patients, we developed a newly designed trunk orthosis that provides resistive force through spring joints.
Objectives: This study aimed to determine the newly designed trunk orthosis’s biomechanical effects during level walking.
Study design: Before-after trials must be better.
Methods: Measurements were taken for nine chronic-phase (>2 years post-onset) stroke patients using a three-dimensional motion capture system and force plates under three experimental conditions: self-selected gait speed without the newly designed trunk orthosis, with the newly designed trunk orthosis, and after newly designed trunk orthosis removal. We analyzed and compared spatiotemporal and kinetic parameters of the paretic and non-paretic limbs and kinematic parameters of the trunk and bilateral limbs.
Results: Several pre-swing gait parameters (e.g. hip joint flexion moment and ankle joint plantar flexion angle) after newly designed trunk orthosis removal were significantly increased compared to those without newly designed trunk orthosis. Step length of the paretic limb tended to increase after newly designed trunk orthosis removal.
Conclusion: The newly designed trunk orthosis effectively modified trunk alignment, but larger improvements in kinetic and kinematic parameters were observed in the bilateral limbs after newly designed trunk orthosis removal than with the newly designed trunk orthosis.
Clinical relevance Stroke patients improved only trunk malalignment while wearing the newly designed trunk orthosis. Gait after newly designed trunk orthosis removal was better than with the newly designed trunk orthosis. Positive changes after removal were mostly observed in pre-swing of the hemiparetic limb. The newly designed trunk orthosis might be effective for gait training in stroke patients.

Wednesday, August 20, 2014

The Chairless Chair, an invisible chair that you can wear

Several prototypes have been constructed: the latest weighs about two kilograms and can operate for 24 hours on battery power.

I could easily see this as being quite useful for stroke survivors. Is your doctor going to suggest this for your ambulatory and fatigue needs?

Although the focus is on production lines, the device has other potential daily life applications.

Video here:

Dr. Edward Tobinick - of etanercept (Enbrel) fame suing a blogger

Dr. Tobinick could easily solve all these problems of his by writing up proof of his clinical research but he goes down the dubious route of suing critics. In my opinion a sign of desperation when truth and facts are not on your side.
I never would have gone down this route anyway, there never was anything other than anecdotes for this as a stroke treatment.

Case docket here:
Dr. Gorski writing about it here;

Can instant noodles lead to heart disease, diabetes and stroke?

Young women are going to have to stop eating ramen and taking birth control. A little alarmist maybe? If they were to study the underlying reason that eating ramen causes this, that would be much more useful than this secondary prevention tactic. Come on, rub a couple of neurons together once in a while. Somebody out there in the stroke medical world has to have a working brain. We may be past the four humors theory but just barely.
Illustration from the book, Minerva Britanna. At the top of the page is the word phlegma, and an illustration of a man sitting next to the fire of a hearth, with a turtle near his feet.


  • Humor: Phlegm
  • Element: Water
  • Season: Autumn
  • Age: Maturity
  • Qualities: Cold & Moist
  • Organ: Brain
  • Planet: Moon
Recent Baylor research shows that significant consumption of the convenient food product – ramen included – may increase a person's risk for cardiometabolic syndrome, especially in women. The findings, recently published in The Journal of Nutrition, could shed new light on the risks of a worldwide dietary habit. Dr. Shin, who led the study on behalf of the Baylor Heart and Vascular Hospital (BHVH), found that eating instant noodles two or more times a week was associated with cardiometabolic syndrome, which raises a person's likelihood of developing heart disease and other conditions, such as diabetes and stroke. Dr. Shin also found that those results were more prevalent in women. He said that can likely be attributed to biological differences (such as sex hormones and metabolism) between the sexes, as well as obesity and metabolic syndrome components. In addition, men and women's varied eating habits and differences in the accuracy of food reporting may play a role in the gender gap. Another potential factor in the gender difference is a chemical called bisphenol A (BPA), which is used for packaging the noodles in Styrofoam containers. Studies have shown that BPA interferes with the way hormones send messages through the body, specifically estrogen. Regardless of the gender–related findings or their causes, Dr. Shin said, the study represents the importance of understanding the foods we feed our bodies.

Global sodium consumption and death from cardiovascular causes

You're going to have to 'trust' your doctor on this one. There is so much conflicting information out there. I've only written 10 posts on it if you want to educate yourself for your doctors meeting.
This seems to be putting one hell of a lot of credence into correlation.  And a second level correlation at that, salt causes high blood pressure, high blood pressure causes cardiovascular disease.
High sodium intake increases blood pressure, a risk factor for cardiovascular disease, but the effects of sodium intake on global cardiovascular mortality are uncertain. In this modeling study, 1.65 million deaths from cardiovascular causes that occurred in 2010 were attributed to sodium consumption above a reference level of 2.0 g per day.
  • Authors collected data from surveys on sodium intake as determined by urinary excretion and diet in persons from 66 countries (accounting for 74.1% of adults throughout the world), and they used these data to quantify the global consumption of sodium according to age, sex, and country.
  • The effects of sodium on blood pressure, according to age, race, and the presence or absence of hypertension, were calculated from data in a new meta–analysis of 107 randomized interventions, and the effects of blood pressure on cardiovascular mortality, according to age, were calculated from a meta–analysis of cohorts.
  • Cause–specific mortality was derived from the Global Burden of Disease Study 2010
  • Using comparative risk assessment, they estimated the cardiovascular effects of current sodium intake, as compared with a reference intake of 2.0 g of sodium per day, according to age, sex, and country.
  • In 2010, the estimated mean level of global sodium consumption was 3.95 g per day, and regional mean levels ranged from 2.18 to 5.51 g per day.
  • Globally, 1.65 million annual deaths from cardiovascular causes (95% uncertainty interval [confidence interval], 1.10 million to 2.22 million) were attributed to sodium intake above the reference level; 61.9% of these deaths occurred in men and 38.1% occurred in women.
  • These deaths accounted for nearly 1 of every 10 deaths from cardiovascular causes (9.5%).
  • Four of every 5 deaths (84.3%) occurred in low– and middle–income countries, and 2 of every 5 deaths (40.4%) were premature (before 70 years of age).
  • The rate of death from cardiovascular causes associated with sodium intake above the reference level was highest in the country of Georgia and lowest in Kenya.

Randomized controlled trial on hemifield eye patching and optokinetic stimulation in acute spatial neglect

I'm sure your doctor will be telling you shortly that this trial failed. But ask anyway about the protocol used to see if you want to try it anyway.
In a randomized controlled trial, the authors compared the combined treatment of hemifield eye patching and repetitive optokinetic stimulation in acute stroke patients with neglect to the spontaneous course. An early intervention of combined hemifield eye patching and optokinetic stimulation in acute stroke patients with spatial neglect has no additive effect to the spontaneous remitting course of the disorder.

Chronic stress, depressive symptoms, anger, hostility, and risk of stroke and transient ischemic attack in the multi-ethnic study of atherosclerosis

They could have just said, 'We know nothing about stroke and don't care. It's not our problem'.
This study investigated chronic stress, depressive symptoms, anger, and hostility in relation to incident stroke and transient ischemic attacks in middle–aged and older adults. Higher levels of stress, hostility, and depressive symptoms are associated with significantly increased risk of incident stroke or transient ischemic attacks in middle–aged and older adults. Associations are not explained by known stroke risk factors.
(Then do some f*cking work and figure out what the risk factor is. God are people lazy. My guess is that these all cause inflammation and inflammation is a known risk factor.)
  • Data were from the Multi-Ethnic Study of Atherosclerosis (MESA), a population-based cohort study of 6749 adults, aged 45 to 84 years and free of clinical cardiovascular disease at baseline, conducted at 6 US sites.
  • Chronic stress, depressive symptoms, trait anger, and hostility were assessed with standard questionnaires.
  • The primary outcome was clinically adjudicated incident stroke or transient ischemic attacks during a median follow-up of 8.5 years.
  • One hundred ninety-five incident events (147 strokes; 48 transient ischemic attacks) occurred during follow-up.
  • A gradient of increasing risk was observed for depressive symptoms, chronic stress, and hostility (all P for trend ≤0.02) but not for trait anger (P>0.10).
  • Hazard ratios (HRs) and 95% confidence intervals indicated significantly elevated risk for the highest-scoring relative to the lowest-scoring group for depressive symptoms (HR, 1.86; 95% confidence interval, 1.16–2.96), chronic stress (HR, 1.59; 95% confidence interval, 1.11–2.27), and hostility (HR, 2.22; 95% confidence interval, 1.29–3.81) adjusting for age, demographics, and site.
  • HRs were attenuated but remained significant in risk factor–adjusted models.
  • Associations were similar in models limited to stroke and in secondary analyses using time-varying variables.

Tuesday, August 19, 2014

Regularly practicing hatha yoga may improve brain function for older adults

Amy, you could contact  the editor with your ideas on meditation.
How to contact the editor
Please send tips or questions toMichelle Brandt. - See more at:
 Please send tips or questions to Michelle Brandt -
She didn't followup my idea of the state of stroke research.

How to contact the editor
Please send tips or questions toMichelle Brandt. - See more at:

Targeted stimulation of specific brain cells boosts stroke recovery in mice

So who is going to take charge of getting this into human clinical trials? We know it is not going to be the ASA, NSA or WSO because obviously their boards of directors have no intention of ever solving any stroke problem.
Only a GREAT STROKE ASSOCIATION will ever tackle all the hardest problems in stroke. 

Physical Fitness Makes Kids' Brains Bigger

Whom is going to follow these for the next 70 years to see if they survive stroke better and end up with less disability?
 This is pretty much what John J. Ratey, MD, author of Spark: The Revolutionary New Science of Exercise and the Brain, wrote about neurogenesis in 2008.
A new study of 9- and 10-year-olds finds that those who are more aerobically fit have more fibrous and compact white-matter tracts in the brain than their peers who are less fit. “White matter” describes the bundles of axons that carry nerve signals from one brain region to another. More compact white matter is associated with faster and more efficient nerve activity. 
The team reports its findings in the open-access journal Frontiers in Human Neuroscience
“Previous studies suggest that children with higher levels of aerobic fitness show greater brain volumes in gray-matter brain regions important for memory and learning,” said University of Illinois postdoctoral researcher Laura Chaddock-Heyman, who conducted the study with kinesiology and community health professor Charles Hillman and psychology professor and Beckman Institute director Arthur Kramer. “Now for the first time we explored how aerobic fitness relates to white matter in children’s brains.”
I was quite physically fit as a kid, walking and biking all over the place.
More at link.

Central pattern generators and the control of rhythmic movements

If these exist why does spasticity override them?
Under an Elsevier user license
  Open Archive


Central pattern generators are neuronal circuits that when activated can produce rhythmic motor patterns such as walking, breathing, flying, and swimming in the absence of sensory or descending inputs that carry specific timing information. General principles of the organization of these circuits and their control by higher brain centers have come from the study of smaller circuits found in invertebrates. Recent work on vertebrates highlights the importance of neuro-modulatory control pathways in enabling spinal cord and brain stem circuits to generate meaningful motor patterns. Because rhythmic motor patterns are easily quantified and studied, central pattern generators will provide important testing grounds for understanding the effects of numerous genetic mutations on behavior. Moreover, further understanding of the modulation of spinal cord circuitry used in rhythmic behaviors should facilitate the development of new treatments to enhance recovery after spinal cord damage.


Biologists often take for granted the rapidity at which new information is acquired. It is humbling, therefore, to reread the papers of the first systems neuroscientists, and to discover among them the first articulation of many of the basic concepts that we still struggle to elucidate today. Almost ninety years ago, Brown [1] suggested that the alternate flexion and extension of leg muscles in walking could be produced by rhythmic central circuits in which the antagonistic muscles were driven by neurons that inhibited each other. Nonetheless, the spinal reflex has dominated a century of textbooks, and many biologists labor under the misconception that rhythmic movements are produced by reflex activation, rather than by central circuits. This review is not intended to supplant or replace the many outstanding and detailed reviews of the organization of the neural control of rhythmic movements in both invertebrates and vertebrates 2., 3., 4., 5. and 6.. Rather, here our purpose is to provide a roadmap to the general principles underlying pattern generation. We hope that this review will be helpful to those looking for neural circuits with easily quantifiable outputs with which to evaluate the role of genes in neuronal function.

Fictive motor patterns show that rhythmic movements can be generated in the absence of sensory input

How does one show the existence of central circuits capable of the production of rhythmic movements? For many years early neuroscientists debated whether rhythmic movements were produced by chains of reflexes or central oscillators (Fig. 1a). The first direct experiments designed to address this question were attempts to cut all sensory feedback to the central nervous system. This is obviously a difficult task, and some of the earliest successful experiments of this kind were carried out by Wilson and colleagues 7., 8. and 9., who showed that a deafferented locust could generate rhythmic flight motor patterns in response to non-rhythmic stimulation of the nerve cord.

Cool images at  the link.

Re-learning Gait After a Stroke

A pretty complete description of gait retraining. My only quibble is the focus on early intensive and repetitive practice. This may have solved my post of Jan. 2013

When should rehabilitation begin after stroke?

But only your doctor can tell for sure, so ask.

Blood pressure medication does not cause more falls

This then refutes this study; Are Blood Pressure Drugs Worth the Falls?
Ask your doctor for an analysis for which one is correct. This latest specifically studied diabetes patients. So have your doctor check that out.
Study on patients with type 2 diabetes examined fracture risk with antihypertensive treatment

It's time to question the common belief that patients receiving intensive blood pressure treatment are prone to falling and breaking bones. A comprehensive study in people ages 40 to 79 with diabetes, led by Karen Margolis, MD, of HealthPartners Institute for Education and Research in the US, found no evidence supporting this belief. The study¹ appears in the Journal of General Internal Medicine², published by Springer.
Evidence from various clinical trials shows that cardiovascular events such as strokes can be prevented by treating high blood pressure (hypertension).. However, physicians and patients still often express concern that its tight control may increase a person's risk of low blood pressure (hypotension) and subsequent falls and fractures.
Scientific data to support this notion are sparse. Therefore, Margolis and her associates compared the number of falls and fractures of type 2 diabetes patients receiving two types of blood pressure treatment. The intensive group (which included 1,534 participants) received treatment aimed at a systolic blood pressure of <120 mm Hg, while the target for the standard group (1,565 participants) was <140 mm Hg.

Participants were all part of ACCORD-BONE, an ancillary study of the Action to Control Cardiovascular Risk in Diabetes (ACCORD) randomized trial, which tested how more intensive treatment of blood sugar, blood pressure and lipids affected cardiovascular disease outcomes in people with diabetes. Participants in the ACCORD-BONE study were, on average, about 62 years old; none were 80 or older.
The results show that patients who received intensive blood pressure treatment did not fall more than less intensively treated patients, nor did they incur more fractures over an average follow-up of about five years.

"Lowering blood pressure using intensive treatment compared with standard treatment did not result in an increased rate of falls or fractures and, in fact, showed possible trends towards fewer fractures in the intensively treated patients," explains Margolis. "Although intensive blood pressure treatment to the low levels in ACCORD did not lower cardiovascular events, our results and review of the literature suggest a need to carefully reconsider current thinking about whether antihypertensive treatment and blood pressure lowering increases risk for falls and fractures."

Results in older versus younger patients were not different. No evidence suggested that the risk of patients' falling varied over time, although there were not enough fractures to determine if the short-term risk might be higher at the beginning of intensive treatment. It is important to note that subjects in this study were more closely monitored than most patients in clinical practice; therefore, the results may not completely reflect what would happen in actual practice.

Hospitalizations, deaths from heart disease, stroke drop in last decade

Has your hospital followed the same trend? No statistics to support or refute that should be a fireable offense for the head of the stroke department. No available statistics from the ASA, NSA or WSO would be a fireable offense there also.
U.S. hospitalizations and deaths from heart disease and stroke dropped significantly in the last decade, according to new research in the American Heart Association journal Circulation.
“Interestingly, these improvements happened in a period when there were no real ‘miracle’ clinical advancements,” said Harlan Krumholz, M.D., S.M., lead author of the “most comprehensive report card to-date” on America’s progress in heart disease and stroke prevention and treatment. “Rather, we saw consistent improvements in the use of evidence-based treatments and medications and an increase in quality improvement initiatives using registries and other data to track performance and support improvement efforts — as well as a strong emphasis on heart-healthy lifestyles and behaviors.”
Researchers collected data on nearly 34 million Medicare Fee-For-Service recipients in 1999-2011. They analyzed trends in rates of hospitalization, dying within a month of being admitted, being admitted again within a month and dying during the following year. They considered patient factors including age, sex, race, other illnesses and geography.
By the end of 2011, hospitalization rates among all races and areas dropped:
  • 38 percent for heart attack;
  • 83.8 percent for unstable angina, sudden chest pain often leading to heart attack;
  • 30.5 percent for heart failure; and
  • 33.6 percent for ischemic stroke.
Furthermore, risks of dying for people who went to the hospital within a year decreased about 21 percent for unstable angina, 23 percent for heart attacks and 13 percent for heart failure and stroke.
“Huge strides in lifestyle, quality of care and prevention strategies for cardiovascular health have seemed to have a ripple effect on saving lives,” said Krumholz, director of the Center of Outcomes Research and Evaluation at Yale-New Haven Hospital in New Haven, Conn. “As a result, our country has undergone remarkable changes, which has reduced suffering and costs.”
Other significant contributions included improvements in identifying and treating high blood pressure, a rapid rise in the use of statins, marked declines in smoking and more timely and appropriate treatment for heart attack patients, he said.
“There is still more work to do as heart disease and stroke combined remain the leading cause of death and disability, but this study documents astonishing progress and national achievement,” Krumholz said.

Endogenous neurogenesis following ischaemic brain injury: Insights for therapeutic strategies

Ask your doctor to create a translational research project with other doctors to figure out what the standard stroke protocol should be for this. They will not do this on their own. YOU have to initiate this and create the expectation that they will follow thru.
If we had a great stroke association it could be handed off to them and the project would get done. But we have press release stroke associations. I don't know how the boards of directors can live with themselves for such pathetic efforts.
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Ischaemic stroke is among the most common yet most intractable types of central nervous system (CNS) injury in the adult human population. In the acute stages of disease, neurons in the ischaemic lesion rapidly die and other neuronal populations in the ischaemic penumbra are vulnerable to secondary injury. Multiple parallel approaches are being investigated to develop neuroprotective, reparative and regenerative strategies for the treatment of stroke. Accumulating evidence indicates that cerebral ischaemia initiates an endogenous regenerative response within the adult brain that potentiates adult neurogenesis from populations of neural stem and progenitor cells. A major research focus has been to understand the cellular and molecular mechanisms that underlie the potentiation of adult neurogenesis and to appreciate how interventions designed to modulate these processes could enhance neural regeneration in the post-ischaemic brain. In this review, we highlight recent advances over the last 5 years that help unravel the cellular and molecular mechanisms that potentiate endogenous neurogenesis following cerebral ischaemia and are dissecting the functional importance of this regenerative mechanism following brain injury.
This article is part of a Directed Issue entitled: Regenerative Medicine: the challenge of translation.


  • Stroke;
  • Neural stem cells;
  • Cell proliferation;
  • Brain repair;
  • Cell signalling
This article is part of a Directed Issue entitled: Regenerative Medicine: the challenge of translation.

Corresponding author at: Florey Institute of Neuroscience and Mental Health, Kenneth Myer Building, 30 Royal Parade, Parkville, VIC 3010, Australia. Tel.: +61 3 90356535; fax: +61 3 86779826.

Corresponding author. Tel.: +61 3 99029622; fax: +61 3 99052766.
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Effect of treatment delay, age, and stroke severity on the effects of intravenous thrombolysis with alteplase for acute ischaemic stroke: a meta-analysis of individual patient data from randomised trials

This makes it sound like tPA is 32.9% effective as compared to 12% from an earlier report. Your doctor should be able to compare their hospital statistics to see if they are least match this better result.  If your hospital doesn't even know how well tPA works then the head stroke doctor should be fired.
Alteplase is effective for treatment of acute ischaemic stroke but debate continues about its use after longer times since stroke onset, in older patients, and among patients who have had the least or most severe strokes. Authors assessed the role of these factors in affecting good stroke outcome in patients given alteplase. Irrespective of age or stroke severity, and despite an increased risk of fatal intracranial haemorrhage during the first few days after treatment, alteplase significantly improves the overall odds of a good stroke outcome when delivered within 4•5 h of stroke onset, with earlier treatment associated with bigger proportional benefits.
  • Authors did a pre–specified meta–analysis of individual patient data from 6756 patients in nine randomised trials comparing alteplase with placebo or open control.
  • They included all completed randomised phase 3 trials of intravenous alteplase for treatment of acute ischaemic stroke for which data were available.
  • Retrospective checks confirmed that no eligible trials had been omitted.
  • They defined a good stroke outcome as no significant disability at 3—6 months, defined by a modified Rankin Score of 0 or 1. (mine was obviously a failure)
  • Additional outcomes included symptomatic intracranial haemorrhage (defined by type 2 parenchymal haemorrhage within 7 days and, separately, by the SITS–MOST definition of parenchymal type 2 haemorrhage within 36 h), fatal intracranial haemorrhage within 7 days, and 90–day mortality.
  • Alteplase increased the odds of a good stroke outcome, with earlier treatment associated with bigger proportional benefit.
  • Treatment within 3•0 h resulted in a good outcome for 259 (32•9%) of 787 patients who received alteplase versus 176 (23•1%) of 762 who received control (OR 1•75, 95% CI 1•35—2•27); delay of greater than 3•0 h, up to 4•5 h, resulted in good outcome for 485 (35•3%) of 1375 versus 432 (30•1%) of 1437 (OR 1•26, 95% CI 1•05—1•51); and delay of more than 4•5 h resulted in good outcome for 401 (32•6%) of 1229 versus 357 (30•6%) of 1166 (OR 1•15, 95% CI 0•95—1•40).
  • Proportional treatment benefits were similar irrespective of age or stroke severity.
  • Alteplase significantly increased the odds of symptomatic intracranial haemorrhage (type 2 parenchymal haemorrhage definition 231 [6•8%] of 3391 vs 44 [1•3%] of 3365, OR 5•55, 95% CI 4•01—7•70, p<0•0001; SITS–MOST definition 124 [3•7%] vs 19 [0•6%], OR 6•67, 95% CI 4•11—10•84, p<0•0001) and of fatal intracranial haemorrhage within 7 days (91 [2•7%] vs 13 [0•4%]; OR 7•14, 95% CI 3•98—12•79, p<0•0001).
  • The relative increase in fatal intracranial haemorrhage from alteplase was similar irrespective of treatment delay, age, or stroke severity, but the absolute excess risk attributable to alteplase was bigger among patients who had more severe strokes.
  • There was no excess in other early causes of death and no significant effect on later causes of death.
  • Consequently, mortality at 90 days was 608 (17•9%) in the alteplase group versus 556 (16•5%) in the control group (hazard ratio 1•11, 95% CI 0•99—1•25, p=0•07).
  • Taken together, therefore, despite an average absolute increased risk of early death from intracranial haemorrhage of about 2%, by 3—6 months this risk was offset by an average absolute increase in disability–free survival of about 10% for patients treated within 3•0 h and about 5% for patients treated after 3•0 h, up to 4•5 h.

Association of poor subjective sleep quality with risk for death by suicide during a 10-year period: a longitudinal, population-based study of late life

Is your doctor doing anything about your sleep problems other than having nurses hand out sleeping pills every night while in the hospital?
Older adults have high rates of sleep disturbance, die by suicide at disproportionately higher rates compared with other age groups, and tend to visit their physician in the weeks preceding suicide death. To authors' knowledge, to date, no study has examined disturbed sleep as an independent risk factor for late–life suicide. To examine the relative independent risk for suicide associated with poor subjective sleep quality in a population–based study of older adults during a 10–year observation period. The results indicate that poor subjective sleep quality is associated with increased risk for death by suicide 10 years later, even after adjustment for depressive symptoms. Disturbed sleep appears to confer considerable risk, independent of depressed mood, for the most severe suicidal behaviors and may warrant inclusion in suicide risk assessment frameworks to enhance detection of risk and intervention opportunity in late life.
  • A longitudinal case–control cohort study of late–life suicide among a multisite, population–based community sample of older adults participating in the Established Populations for Epidemiologic Studies of the Elderly.
  • Of 14 456 community older adults sampled, 400 control subjects were matched (on age, sex, and study site) to 20 suicide decedents.
  • Primary measures included the Sleep Quality Index, the Center for Epidemiologic Studies–Depression Scale, and vital statistics.
  • Hierarchical logistic regressions revealed that poor sleep quality at baseline was significantly associated with increased risk for suicide (odds ratio [OR], 1.39; 95% CI, 1.14–1.69; P < .001) by 10 follow–up years.
  • In addition, 2 sleep items were individually associated with elevated risk for suicide at 10–year follow–up: difficulty falling asleep (OR, 2.24; 95% CI, 1.27–3.93; P < .01) and nonrestorative sleep (OR, 2.17; 95% CI, 1.28–3.67; P < .01).
  • Controlling for depressive symptoms, baseline self–reported sleep quality was associated with increased risk for death by suicide (OR, 1.30; 95% CI, 1.04–1.63; P < .05)

Triglycerides and cardiovascular disease

Once again I would argue that these people don't know cause and effect. Cholesterol doesn't cause cardiovascular disease. It is used to create plaque because of inflammation of the artery lining. The cause is whatever starts that inflammation. Solve that and all this crap about statins and cholesterol probably goes away. They aren't even looking at the right problem. Does nobody rub two brain cells together ever?
After the introduction of statins, clinical emphasis first focussed on LDL cholesterol–lowering, then on the potential for raising HDL cholesterol, with less focus on lowering triglycerides.
  • However, the understanding from genetic studies and negative results from randomised trials that low HDL cholesterol might not cause cardiovascular disease as originally thought has now generated renewed interest in raised concentrations of triglycerides.
  • This renewed interest has also been driven by epidemiological and genetic evidence supporting raised triglycerides, remnant cholesterol, or triglyceride–rich lipoproteins as an additional cause of cardiovascular disease and all–cause mortality.
  • Triglycerides can be measured in the non–fasting or fasting states, with concentrations of 2—10 mmol/L conferring increased risk of cardiovascular disease, and concentrations greater than 10 mmol/L conferring increased risk of acute pancreatitis and possibly cardiovascular disease.
  • Although randomised trials showing cardiovascular benefit of triglyceride reduction are scarce, new triglyceride–lowering drugs are being developed, and large–scale trials have been initiated that will hopefully provide conclusive evidence as to whether lowering triglycerides reduces the risk of cardiovascular disease.
Cool video of the problem here;
Inflammation In Atherosclerotic Plaque Formation

Extravirgin olive oil consumption reduces risk of atrial fibrillation

I haven't been following A-fib much so this one is up to you.
The authors assessed the effect of these diets on the incidence of atrial fibrillation in the PREDIMED trial. In the absence of proven interventions for the primary prevention of atrial fibrillation, this post hoc analysis of the PREDIMED trial suggests that extravirgin olive oil in the context of a Mediterranean dietary pattern may reduce the risk of atrial fibrillation.
  • Participants were randomly assigned to 1 of 3 diets: Mediterranean diet supplemented with extravirgin olive oil, Mediterranean diet supplemented with mixed nuts, or advice to follow a low-fat diet (control group).
  • Incident atrial fibrillation was adjudicated during follow-up by an events committee blinded to dietary group allocation.
  • Among 6705 participants without prevalent atrial fibrillation at randomization, they observed 72 new cases of atrial fibrillation in the Mediterranean diet with extravirgin olive oil group, 82 in the Mediterranean diet with mixed nuts group, and 92 in the control group after median follow-up of 4.7 years.
  • The Mediterranean diet with extravirgin olive oil significantly reduced the risk of atrial fibrillation (hazard ratio, 0.62; 95% confidence interval, 0.45–0.85 compared with the control group).
  • No effect was found for the Mediterranean diet with nuts (hazard ratio, 0.89; 95% confidence interval, 0.65–1.20).

Monday, August 18, 2014

Stem cells for neonatal stroke- the future is here

When is the future for the rest of us survivors?
ASA - Dr. Mariell Jessup,  Whom are you going to assign to this task?

NSA - Mr. Baranski, Whom are you going to assign to this task?

WSO - Dr. Stephen Davis, Whom are you going to assign to this task?

Stem Cells

In recent years stem cell therapy has emerged as a potential treatment for neonatal ischemic brain injury. The efficacy of cell- based therapies in restoring damaged brain tissue has been tested in a multitude of models for different CNS diseases. Several different stem and progenitor cell populations have been utilized as cell-based therapy, including neural stem cells, embryonic stem cells, human umbilical cord blood cells (HUBCs), hematopoietic stem and progenitor cells, and mesenchymal stem cells (MSCs). Most stem cell types appear to enhance recovery to some extent (Pimentel-Coelho and Mendez-Otero, 2010). However, because of their low immunogenicity, availability and positive results obtained from preclinical studies, MSCs are a particularly promising candidate to repair the devastating effects that are associated with neonatal stroke. MSCs were first isolated and identified in bone marrow, but can now be isolated from many tissues, including adipose tissue, muscle, skin and extraembryonic tissues like the placenta, umbilical cord and Wharton's jelly. The latter sources are of particular interest for neonates that experience an ischemic event around the time of birth, at which time cells can be harvested and transplanted from an autologous source. MSCs derived from different sources have slightly different characteristics, but as of yet it is unknown whether this influences their therapeutic potential.
Our group and others have shown that administration of MSCs reduces lesion volume, provides positive effects on the white matter and improves motor function (van Velthoven et al., 2012). Numerous studies have been done under the premise that transplanted stem cells contribute to brain repair by directly replacing damaged or lost tissue. While there is evidence that transplanted cells undergo differentiation toward neuronal lineages, improved outcomes have been observed even when survival of transplanted cells is low and engrafted cells are absent. This suggests that rather than replacing damaged cells, transplanted cells may improve outcome via indirect mechanisms. For example, MSCs have been shown to secrete many factors that can influence important processes like apoptosis, neurogenesis, angiogenesis and synaptogenesis.

More pages at link.

Sickest Reap Greatest Gain From BP Treatment

Have these doctors considered the overall health of these patients?  Don't listen to me I'm obviously stroke addled to even consider questioning the medical gods.
Are Blood Pressure Drugs Worth the Falls?

Low blood pressure and dementia in elderly people: the Kungsholmen project

Claudia Kawas: If you have high blood pressure, it looks like your risk of dementia is lower.

And for you stroke survivors, does your doctor know about any of these?
1. Detrimental effect of blood pressure reduction in the first 24 hours of acute stroke onset
 2. Early Intensive Blood-Pressure Lowering Improves Recovery in Patients With Acute Intracerebral Haemorrhage
 3.  Systolic Blood Pressure During Acute Stroke Is Associated With Functional Status and Long-term Mortality in the Elderly
 4. External Counterpulsation Augments Blood Pressure and Cerebral Flow Velocities in Ischemic Stroke Patients With Cerebral Intracranial Large Artery Occlusive Disease

 Sickest Reap Greatest Gain From BP Treatment

Education Level and Inequalities in Stroke Reperfusion Therapy Observations in the Swedish Stroke Register

This just proves that tPA should be considered a complete failure and something better found. Beating a dead horse is not going to make it race any faster. And yet I bet our stroke medical world will continue down the same failed path for years to come. Unless we overthrow them all.  Notice that they don't talk about results(how many fully recovered due to tPA?). They talk about reperfusion as if that is the important thing to measure. It's not. 
GAH!!! The Stupidity.
  1. Marie Eriksson, PhD
+ Author Affiliations
  1. From the Departments of Public Health and Clinical Medicine (A.S., E.-L.G., K.A.) and Statistics (M.E.), Umeå University, Umeå, Sweden; and Department of Clinical Sciences, Section of Neurology, Lund University, Lund, Sweden (B.N.).
  1. Correspondence to Anna Stecksén, RPT, MSc, Department of Public Health and Clinical Medicine, Umeå University, S-901 87 Umeå, Sweden. E-mail


Background and Purpose—Previous studies have revealed inequalities in stroke treatment based on demographics, hospital type, and region. We used the Swedish Stroke Register (Riksstroke) to test whether patient education level is associated with reperfusion (either or both of thrombolysis and thrombectomy) treatment.
Methods—We included 85 885 patients with ischemic stroke aged 18 to 80 years registered in Riksstroke between 2003 and 2009. Education level was retrieved from Statistics Sweden, and thrombolysis, thrombectomy, patient, and hospital data were obtained from Riksstroke. We used multivariable logistic regression to analyze the association between reperfusion therapy and patient education.
Results—A total of 3649 (4.2%) of the patients received reperfusion therapy. University-educated patients were more likely to be treated (5.5%) than patients with secondary (4.6%) or primary education (3.6%; P<0.001). The inequality associated with education was still present after adjustment for patient characteristics; university education odds ratio, 1.14; 95% confidence interval, 1.03 to 1.26 and secondary education odds ratio, 1.08; 95% confidence interval, 1.00 to 1.17 compared with primary education. Higher hospital specialization level was also associated with higher reperfusion levels (P<0.001). In stratified multivariable analyses by hospital type, significant treatment differences by education level existed only among large nonuniversity hospitals (university education odds ratio, 1.20; 95% confidence interval, 1.04–1.40; secondary education odds ratio, 1.14; 95% confidence interval, 1.01–1.29).
Conclusions—We demonstrated a social stratification in reperfusion, partly explained by patient characteristics and the local hospital specialization level. Further studies should address treatment delays, stroke knowledge, and means to improve reperfusion implementation in less specialized hospitals.