Deans' stroke musings

Changing stroke rehab and research worldwide now.Time is Brain!Just think of all the trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 493 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It's quite disgusting that this information is not available from every stroke association and doctors group.
My back ground story is here:

Sunday, January 31, 2016

Stroke Research: Current Advances and Future Hopes

Have your doctor submit their research to this journal, Journal of International Medical Research (JIMR. No research, then call up the hospital president and ask what the hell the objectives are for the stroke department head to stay employed. Because the status quo is totally unacceptable. I'm not ok with how poorly I and most other survivors are recovering.  Don't let them get away with the lazy excuse, 'All strokes are different, all stroke recoveries are different'. Anyone who says that needs to be keel hauled.
New Special Issue - Open for submissions now
“Stroke Research: Current Advances and Future Hopes”
We are pleased to let you know manuscript submissions are now being taken for the 2016 Special Issue on “Stroke research: current advances and future hopes”, publishing in Journal of International Medical Research (JIMR) and guest edited by Dr Auwal Abdullahi of Department of Physiotherapy, Bayero University Kano, Nigeria. If this sounds like the right fit for your research, we would be delighted to receive your paper for review.
Submit Your Article Online >>

Submit your manuscript icon
Submit your manuscript
Are you ready to submit your manuscript? Visit our manuscript submission portal.
About the journal icon
About the journal
JIMR is an open access journal with an Impact Factor of 1.438*.
*Source: 2014 Journal Citation Reports® (Thomson Reuters, 2015)
Open Access FAQ icon
Editorial Board
Find out more about the JIMR Editors and Editorial Board members.

Submit to this Special Issue today
Potential topics for the Special Issue could include, but are not limited to:
  • Stroke prevention and health promotion
  • Current advances in the medical management of stroke
  • Risk factors for stroke
  • Stroke complications
  • Motor rehabilitation after stroke
  • Cognitive rehabilitation
  • Gait rehabilitation
  • Balance rehabilitation
The submission deadline is 25th March 2016.
Submitting your manuscript to the journal is free, and all submissions will be fully peer-reviewed as rapidly as possible. If your manuscript is accepted then you will be asked to pay the page charge, which currently stands at the rate of £325 (+VAT where applicable) per printed journal page, assuming no colour figures (colour figures are subject to an additional fee).
For advice on submitting your manuscript, visit the Manuscript Submission Guidelines for more information. Please don't hesitate to get in touch with any questions you may have regarding this Special Issue.
Kind Regards,

Professor Malcolm H. Lader, OBE, LLB, DSc, PhD, MD, FRCPsych, FMed Sci Editor, Journal of International Medical Research

Saturday, January 30, 2016

Poor diet, smoking contribute to increase in young stroke patients

But they don't point our marijuana like others who have an agenda and axe to grind.

Smoking high-strength cannabis may damage nerve fibres in brain

Vessel Blockage Common in Young Stroke Patients Who Smoke Pot


The latest here:

Poor diet, smoking contribute to increase in young stroke patients

'We have a strategic plan, it's called doing things' - Herb Kelleher

Founder of Southwest Airlines. I know our stroke associations don't have any strategic plan at all, they are just letting all future survivors recover just as badly as you did.  But you can buy this print from to remind you that your children and grandchildren are screwed unless WE change stroke leadership.

Friday, January 29, 2016

Brain Preservation Foundation

Considering the fact that we have no clue how to change the brain to recover from a stroke I can't see any way that the existing technology would be able to chemopreservation or cryopreservation  a brain today in the hope that successful reanimation will be figured out in the future.

MAGIC Post-Stroke Project - Dublin City University

This seems to be a wonderful project, but it is not attacking the primary problem only the secondary problem of delivering support to survivors. If we had ANY stroke leadership at all we would tackle the primary problem; dead and dying neurons as a result of the stroke. Stopping the neuronal cascade of death would help survivors much more than this effort but isn't as photogenic or as easy.

MAGIC Post-Stroke Project - Dublin City University

DCU Business School academics, Professor Regina Connolly and Dr Paul Davis, have been successful in attracting large EU funding in relation to the MAGIC Post-Stroke Project. The project aims to enable significant change in the delivery of health and social care services for patients post stroke.
Over 508,000 EU citizens are in need of post stroke services every year. Due to demographic changes, the health and social care systems are failing to keep pace with demand. The MAGIC Post-Stroke Project has recognised this significant gap associated with the recovery and needs of people post stoke.
“Presently one third of all stroke patients are discharged from hospital with a significant change to life-style, well-being, health status and independence, yet community health and social care services don’t enable patients to make a sufficient recovery post stroke.” said Professor Regina Connolly.
There has been significant progress in developing state of the art technologies to assist patients. However, there has been no system to implement rehabilitative improvement at scale or integrate health and social care services. MAGIC will use pre-commercial procurement to engage industry providers who will be required to compete through several phases of solution development and testing.
Professor Connolly explained: “By working in new ways and by reengineering systems with novel, innovative technology and solutions, we can think differently about our approach to care and improve the well-being of patients, optimising the opportunity for recovery post stroke.”
Dr Paul Davis commented: “MAGIC is an essential and strategically critical programme to modernise health and social care systems to meet demand and to stimulate research, development and innovation which will ultimately help a care team optimise a patient’s recovery.  MAGIC will also stimulate European industry to become a global leader in this innovative field.”
The total cost of the project will be over €5.1 million Euro, with 70 per cent funded by H2020, the EU’s programme for research and innovation. The MAGIC project will run until 2019. Partners include the University of Ulster, the UK Regional Health and Social Care Board, Invest NI and partners in the Czech Republic, Denmark, Finland, Italy, Luxembourg and Spain.


I bet whatever this bottle contained did at least as much good as what your neurologist is recommending today to get you cured from your paralysis.

This link displays what the stuff was supposed to do for you. 21% alcohol. $1.00 per bottle. 1886 patent.
Notices of Judgment Under the Food and Drugs Act, Issue 4001; Issue 5000

Thursday, January 28, 2016

How well is stroke care being provided at your local hospital? UK

Guargantuan F*cking Whoopee.

Notice they say domains of care NOT results. If they don't measure results they will NEVER be able to solve the problems. This is basically worthless, throw it back in their face, I don't give a shit how many MDs and PhDs wrote this, this doesn't help survivors now or in the future. You have to advocate for much better than this to pay it forward for future survivors.  These people are still sitting on their asses not helping.
These tables provide a summary of performance for named teams based on 10 domains of care. Each domain is given a performance level (level A to E) and a key indicator score is calculated based on the average of the 10 domain levels for both patient-centred and team centred domains. A Combined Key Indicator (KI) Score is derived from the average of the patient- and team-centred total KI score which is adjusted for case ascertainment and audit compliance level to give a final overall SSNAP level.

The effects of diabetes, hypertension, asthma, heart disease, and stroke on quality-adjusted life expectancy

No clue where 12.4 figure comes from, I've only seen
brain injury patients were estimated to be around five years older on average than their real age.



Quality-adjusted life expectancy (QALE) is a summary measure that combines mortality and health-related quality of life across different stages of life. The objective of this study was to estimate QALE loss due to five chronic diseases-diabetes mellitus, hypertension, asthma, heart disease, and stroke.


Health-related quality of life scores were from the 1993-2009 Behavioral Risk Factor Surveillance System. Using age-specific deaths from the Compressed Mortality File, this study constructed life tables to calculate losses in life expectancy and QALE due to each of the five diseases from 1993 through 2009 and for 50 US states and the District of Columbia.


In 2009, the individual-level QALE loss for diabetic people, compared with nondiabetic people, was 11.1 years; for those with hypertension, 6.3 years; for those with asthma, 7.0 years; for those with heart disease, 10.3 years; and for those with stroke, 12.4 years. At the population level, diabetes, hypertension, asthma, heart disease, and stroke contributed 1.9, 2.2, 0.8, 1.2, and 0.8 years of population QALE loss at age 18 years, respectively.


Persons with each of the five diseases had significantly lower life expectancy and QALE. Because the prevalence of diabetes and hypertension has increased significantly in the United States in the last two decades, the burdens of these two conditions, measured by population QALE losses, had increased 83% and 29% from 1993 to 2009, respectively. Also, by examining changes in population QALE loss at different ages, policymakers can identify age groups most affected by particular diseases and develop the most cost-effective interventions by focusing on these groups.
Copyright © 2013 International Society for Pharmacoeconomics and Outcomes Research (ISPOR). Published by Elsevier Inc. All rights reserved.
[PubMed - indexed for MEDLINE]


Free PMC Article

American Heart Association And HealthSouth Chattanooga Rehabilitation Hospital Join ‘Together To End Stroke’

What a fucking lazy waste. PRESS RELEASES!!!

Guargantuan F*cking Whoopee.

If you really want to help survivors you will sponsor research into solving all the problems in stroke. But that would mean actual hard work, writing up research proposals, writing up grant proposals to fund that research. You local people need to start screaming at these 'leaders'. What the hell is the point of getting fast to a stroke hospital when tPA fully works only 12% of the time. It can save your life but does nothing to stop the neuronal cascade of death. Look how large my dead area is and I got tPA in 90 minutes. By going down this route the AHA and HealthSouth have to do absolutely nothing, the press releases are canned.
The American Heart Association and HealthSouth Chattanooga Rehabilitation Hospital have partnered to support the American Heart Association "Together to End Stroke" campaign in the Tennessee Valley.
"Throughout the year, the two organizations will launch new education programs for the local community that will help generate awareness and prevention for the number 4 killer and number one disabler of Americans," organizers said.

As part of this awareness campaign, the American Heart Association and HealthSouth Chattanooga Rehabilitation Hospital will teach the acronym F.
A.S.T. to help people recognize the warning signs of a stroke. F.A.S.T. stands for:

F - Face Drooping: Does one side of the face droop or is it numb?

A - Arm Weakness: Is one arm weak or numb?

S - Speech Difficulty: Is speech slurred, are they unable to speak, or are they hard to understand?

T - Time to call 9-1-1: If the person shows any of these symptoms, even if the symptoms go away, call 9-1-1 and get them to the hospital immediately.

“I’m proud that our organization is teaming up with the American Heart Association for  ‘Together to End Stroke,’ said Scott Rowe, CEO of HealthSouth Chattanooga Rehabilitation Hospital. “Every 40 seconds, one of our siblings, grandparents, neighbors or coworkers has a stroke.  While we are helping stroke survivors recover from devastating effects of stroke and regain their independence, we also realize that knowing the warning signs of stroke can dramatically affect the health outcomes of those experiencing one.”

The American Heart Association and American Stroke Association’s Together to End Stroke initiative aims to educate all Americans that stroke is largely preventable, treatable and beatable. Through Together to End Stroke, efforts are focused on increasing awareness and driving action among Americans across the entire stroke continuum of care; prevention, acute treatment, and post-stroke rehabilitation.

"HealthSouth Chattanooga Rehabilitation Hospital and the American Heart Association want everyone in the Tennessee Valley to know the major stroke risk factors and how to reduce their risk, and the F.A.S.T. warning signs and the importance of calling 911 at the first sign of a stroke to minimize the long-term of effects of a stroke and even prevent death. By doing this, HealthSouth Chattanooga Rehabilitation Hospital and the American Stroke Association can directly impact lives in our community," officials said.

“Together, we can keep our loved ones – and their hearts – healthy for years to come,” said Mr. Rowe.

My supplement and diet regime

Do not follow this. There is no clinical proof that any of this works. There is initial research that I refer to but since we have NO leadership and NO strategy we will never find out what we should be eating post-stroke. Right now there is no way to easily measure if the endpoints of all this are working as expected.
1. chocolate - 80%+ cocoa, 2 pieces

CV prevention with dark chocolate 

2. beets, I do pickled because I can't stand cooked beets, they taste like my Moms. 4-5 oz.

New research suggests beets could help increase blood flow to the brain .


Beet Juice Beats Hypertension


Beet Juice Lowers Blood Pressure


3. tomatoes - fresh, not cooked

Lycopene in tomatoes reduces stroke risk by more than 50%

4. olive oil, used with balsamic vinegar for bread dipping.

Research proves that vegetables fried with olive oil have more healthy properties than boiled ones


Extravirgin olive oil consumption reduces risk of atrial fibrillation


To improve memory and thinking skills, try the Mediterranean diet with added olive oil and nuts


5 Healthy Eating Habits to Steal From Europeans


Olive oil cuts risk of stroke by 41 percent





5. Cranberry/pomegranate juice

Pomegranate juice consumption for 3 years by patients with carotid artery stenosis reduces common carotid intima-media thickness, blood pressure and LDL oxidation 


Cranberry juice consumption may protect against cardiovascular disease


Drinking low-calorie cranberry juice may help lower risk of heart disease, diabetes and stroke

6. greek yogurt - probiotics

Effect of Probiotics on Blood Pressure

Consumption of Fermented Milk Product With Probiotic Modulates Brain Activity


7. coffee - many cups

Moderate coffee drinking may be linked to reduced risk of death


Coffee associated with colon cancer survival


Good News: Coffee Could Be Cleaning Out Your Arteries.


Consuming one cup of coffee per day can decrease stroke risk by up to 20%.


 Does More Coffee Mean Less Arterial Plaque? -Arterial calcium lowest in healthy Korean adults with moderate-to-heavy coffee habits.


Coffee associated with colon cancer survival


How A Cup Of Coffee May Help People Manage Stress, Avoid Depression And Memory Loss 


Coffee May Lower Your Risk of Dementia 


How coffee protects against Parkinson’s


Usual dose of caffeine has a positive effect on somatosensory related postural stability in hemiparetic stroke patients


Drinking Coffee Can Lower Alzheimer's Risk By 20%, All It Takes Is 3 Cups A Day


8. coconut oil, added to chai and for frying eggs, for grilled cheese sandwiches instead of margarine.

Evidence-Based Medicinal Properties of Coconut Oil - brain boosting  

9. Aged garlic extract, 2400mg day

New study shows aged garlic extract can reduce dangerous plaque buildup in arteries

10. Fish oil - Omega-3

Fish Oil Might Guard Against Loss of Brain Cells

Omega 3 fatty acid for the prevention of cognitive decline and dementia

11. tocotrienol

Palm tocotrienols can prevent brain cell death after stroke

12. almonds

New research shows almonds reduce the risk of heart disease


13. oatmeal

10 Foods to Calm Inflammation

14. watermelon, approximately 1 pound a day since I couldn't find juice.

Watermelon juice reverses hardening of the arteries  

15. Red wine

Can Wine Protect You From Having a Stroke?

16. Beer

The Close Ties Between Exercise and Beer


Women with moderate beer consumption run lower risk of heart attack


Guinness could really be good for you


If you're over 60, drink up: Alcohol associated with better memory


Beer compound could help fend off Alzheimer’s - hops  


Dark beer is good for you, in moderation


I'm obviously not doing this very well since I'm still 35 lbs. above my ideal weight. I won't stop my dinners out and wine parties because the social connections are needed.

Stroke Rounds: Lesion Site Affects Reperfusion Benefit With Clot Grabber

If the ICA is blocked is it even a stroke since that is prior to entering the Circle of Willis? And if the Circle of Willis is complete then that wouldn't cause problems. Is this problem even defined correctly?
The magnitude of functional outcome benefits from reperfusion with endovascular thrombectomy may depend on the site of occlusion, a meta-analysis showed.
Reperfusion was associated with 3.5-fold higher odds of a good functional outcome (0-2 on the modified Rankin Scale) at 90 days among patients with internal carotid artery (ICA) occlusions and 6.2-fold higher among those with proximal middle cerebral artery (MCA) occlusions versus persistent occlusion.
Reperfusion had no significant association with good functional outcome in distal MCA lesions (OR 1.4, 95% confidence interval 0.8-2.6), although there was a link in the M2 occlusion subset (OR 2.2, 95% CI 1.0-4.7), Robin Lemmens, MD, PhD, of University Hospitals Leuven in Belgium, and colleagues reported online in Neurology.
"The association between reperfusion and good clinical outcomes is stronger in patients with proximal(closer) occlusions compared to distal(farther) occlusions," the group concluded. "Our results, however, do not indicate that patients with distal MCA occlusions do not benefit from endovascular therapy."
"In contrast, the results underscore the need for additional clinical trial data to determine the effect of endovascular therapy in this subgroup," they continued.
Indeed, the study "is not going to change my practice," Haitham Dababneh, MD, of Doctors Hospital at Renaissance in Edinburg, Texas, told MedPage Today. He likewise called for better data from randomized controlled trials, noting differing baseline characteristics between groups in the meta-analysis and the fact that there were fewer patients with distal strokes than proximal strokes.
For now, "it's hard to compare apples to oranges," Dababneh said.
As for the reason why patients with distal MCA occlusions might show less benefit from reperfusion, the authors suggested that those individuals "have less brain tissue at risk of infarction (i.e., less brain tissue that can be salvaged with reperfusion) compared to patients with more proximal MCA or ICA occlusions."
Lemmens and colleagues pooled patient-level data from four large endovascular trials -- SWIFT, STAR, DEFUSE 2, and IMS III -- for a total of 710 patients in their analysis.
Panagiotis Papanagiotou, MD, of Hospitals Bremen-Mitte in Germany, told MedPage Today that clinicians should focus on careful patient selection, perhaps with advanced imaging techniques.
Papanagiotou, who was an investigator for SWIFT, added that the improvement of endovascular techniques -- such as "direct thrombus aspiration to achieve higher recanalization rates" -- may also be helpful for the treatment of distal lesions.

Infrared sauna

This could be so much fun if it works as a stroke therapy. But first we need some fucking leadership that will followup this with research. 

Would heat work  as a stroke therapy?

Extra sensation therapy by feeling all that sweat on your skin, including it running down your back and armpits. You can practice new movements, wiping sweat from your brow with your affected hand.


Frequent saunas may boost survival, Finnish study suggests


New Study Discovers Near-Infrared Light Therapy (NILT) Effectively Treats Traumatic Brain Injury (TBI) Patients


Light therapy could improve brain function in TBI, PTSD


Stroke Rounds: Light Therapy Flopped in Acute Stroke


Near-infrared Spectroscopy–mediated Neurofeedback Enhances Efficacy of Motor Imagery–based Training in Poststroke Victims


What is an infrared sauna? Does it have health benefits?

Neurologist Care Is More Expensive But Delivers Better Results

Really? You will notice they didn't talk in detail about stroke. A great stroke association would complete that analysis for stroke survivors.
An analysis funded by the AAN found that while care for chronic conditions by neurologists costs more than care by other physicians, outcomes tend to be better.
Image Tools
Care by a neurologist for chronic conditions may cost more up front, but it can help reduce emergency department visits, hospitalizations, and medical problems such as infections and fractures, according to an analysis of a large insurance claims database published in the December 23 online edition of Neurology.
The study also found that patients seen by neurologists for chronic neurologic diseases such as multiple sclerosis (MS), Parkinson's disease (PD), or epilepsy are more likely to get disease-modifying treatments than patients who don't see neurologists.
The new study, funded by the AAN, comes amid growing pressure on physicians and other health care providers to demonstrate that their services provide value from both a monetary and outcomes standpoint.
“When we [neurologists] are involved with care, the costs of that care are a little bit more, but at the same time the outcomes are substantially better and the quality of care is better,(But what about results?) said John P. Ney, MD, MPH, the study's lead author and staff neurologist at the Edith Nourse Rogers Memorial Veterans Hospital in Bedford, MA.
The study is part of an ongoing AAN effort to quantify the value of neurologist care. “Aggregation of health care information in large administrative claims databases presents an opportunity to assess the effect of specialist physicians on downstream usage of health resources related to the disease they treat,” the researchers wrote. “Payers, from the US Government to [third-party] private insurers and employers, are looking to this kind of big data analysis to inform coverage decisions, regulatory actions, and policymaking decisions.”
Back to Top | Article Outline


The results may have looked like an argument against neurology if the investigators had only analyzed attributable direct health care expenditures for neurologic conditions, said Dr. Ney. But a different story emerged when the researchers considered factors such as adverse events, hospitalizations, and emergency department visits.
“Neurologist ambulatory care is associated with decreased adverse events and usage of acute and post-acute health care resources,” they concluded. In addition, all-cause hospitalizations were less common for patients seen by a neurologist, which “suggests neurologist visits may have beneficial effects even outside of the treated neurological disorder.”
When neurologists were involved in care, for example, MS patients had fewer urinary tract infections and decubitis ulcers; MS and PD patients experienced fewer pneumonias and less major depression; and PD patients used less home health agency care.The researchers did not attach dollar amounts to the differences in utilization of acute and post-acute care, but they plan to do so in future research, Dr. Ney said.
The study also focused on the use of disease-specific treatments and screenings. For most of the conditions, neurologists seemed to improve care through the use of therapies considered to be optimal treatments. For example, MS patients were more likely to be given immunotherapy; stroke patients with atrial fibrillation were more likely to be given anticoagulants; epilepsy patients were more likely to get deep brain stimulation; and those with Parkinson's were more likely to get dopaminergic therapies.
Having a neurologist involved made no obvious difference in some cases. For instance, “yearly ophthalmologic screening and liver function and blood count testing in MS (if using immune therapies), physical and occupational therapy for PD, and medication compliance rates in epilepsy and MS were not substantially different or slightly worse in the group with identified neurologist care,” the study found.
The researchers said it was not surprising that costs were higher with neurologist care, noting that the goal of health care is “not to provide care at zero or net negative expenditure, but rather to improve health and quality of life at acceptable costs.”
The study did have limitations. The authors noted that it could not adequately adjust for differences in the severity of patients' conditions, and absent information on all acute care expenditures (including those outside the episode treatment groups), it was impossible to say how much money may have been saved. Also, while it makes sense that seeing a neurologist and using disease-specific therapies would lead to higher quality of care and better outcomes, the study was not designed to prove that hypothesis.

Growth Factor in Brain Tied to Slower Mental Decline

How is your doctor testing and making sure your BDNF is adequate?
Older people with higher amounts of brain-derived neurotrophic factor (BDNF) also had slower decline in their memory and thinking abilities than people with lower amounts of the protein, according to a study published in the January 27, 2016, online edition of the journal Neurology.
“This relationship was strongest among the people with the most signs of Alzheimer’s disease pathology in their brains,” said Aron S. Buchman, MD, Rush University Medical Center, Chicago, Illinois. “This suggests that a higher level of protein from BDNF gene expression may provide a buffer, or reserve, for the brain and protect it against the effects of the plaques and tangles that form in the brain as a part of Alzheimer’s disease.”
For the study, 535 people with an average age of 81 years were followed until death, for an average of 6 years. They took yearly tests of their thinking and memory skills, and after death, a neurologist reviewed their records and determined whether they had dementia, mild cognitive impairment (MCI) or no thinking and memory problems.
Autopsies were conducted on their brains after death, and the amount of protein from BDNF gene expression in the brain was then measured. The participants were part of the Rush Memory and Aging Project and the Religious Orders Study.
The rate of cognitive decline was about 50% slower for those in the highest 10% of protein from BDNF gene expression compared with the lowest 10%. The effect of plaques and tangles in the brain on cognitive decline was reduced for people with high levels of BDNF. In the people with the highest amount of Alzheimer’s disease hallmarks in their brains, cognitive decline was about 40% slower for people with the highest amount of protein from BDNF gene expression compared with those with the lowest amount.
On average, thinking and memory skills declined by about 0.10 units per year on the tests. Higher levels of protein from BDNF gene expression reduced the effect of plaques and tangles in the brain on cognitive decline by 0.02 units per year.
The researchers found that the plaques and tangles in the brain accounted for 27% of the variation in cognitive decline, demographics accounted for 3%, and BDNF accounted for 2%.
“More research is needed to confirm these findings, determine how this relationship between protein produced by BDNF gene expression and cognitive decline works and see if any strategies can be used to increase BDNF in the brain to protect or slow the rate of cognitive decline,” said Dr. Buchman.
He noted that the study does not prove that BDNF is the cause of a slower rate of cognitive decline; further work is needed to determine if activities which increase brain BDNF gene expression levels protect or slow the rate of cognitive decline in old age.
In an accompanying editorial, Michal Schnaider Beeri, PhD, Icahn School of Medicine at Mount Sinai, New York, New York, noted that exercise has been shown to increase levels of BDNF in the blood, but that the relationship between BDNF protein levels in the blood and in the brain is not clear.
SOURCE: American Academy of Neurology

Wednesday, January 27, 2016

Free Stroke Rehabilitation Pilot Project - Toronto Canada

Go for it. Say you heard about it from Dean.

 Conductive Education Stroke Rehabilitation Pilot Project

March 14 - 24, 2016

9 classes / 2 hours each

This pilot project is for adults who have survived a stroke who would like to improve mobility and independence.

The goal of the free Stroke Pilot Project is to look at the quality of life (QOL) of stroke survivor’s pre-during-post Conductive Education. All participants in the pilot project will be required to fill in a QOL survey before the intensive, at the end of the intensive and 3 months post intensive. This will assist us look at how Conductive Education can help improve people’s independence and the transfer of learnt skills into the home. 

Eligibility criteria: 

  • The program is open to adults (18+) who have survived a stroke and who are interested in improving their independence and mobility. 
  • Candidates must be currently able to weight bear and transfer with minimal assistance. 
  • Candidates must be able to use washroom independently or bring a caregiver to help with activities of daily living. 
  • For the pilot project we are looking for stroke survivors that have not attended Conductive Education before and that are in good health (no medical conditions that would restrict them from participating fully in the classes). 
  • Able to attend 1 hour selection interview 
  • Able to attend all 9 classes 
  • Successful candidate must complete pre and post study questionnaire and follow up questionnaire 3 months post participation. 
  • Travel arrangement and cost is the responsibility of the candidate 


March of Dimes Canada Head Office
10 Overlea Blvd East York, Toronto, M4H 1 A4 

Frequently Asked Questions

How many classes?
Over the course of two weeks we will run 9 classes (Monday- Friday, no class on Good Friday). 

Has it been too long since I had my stroke? 

No, we have had people in the program a few months post stroke, all the way up to years post stroke. 

Is the building accessible? 

Yes, there is accessible access from the front and back of the building with accessible parking in the back parking lot. There are also plenty of accessible washrooms. 

What happens if I miss a class? 

To be eligible for the pilot program you must commit to attending the full nine classes. There will be no make-up classes for missed or canceled classes. 

What’s the registration process? 

  1. Complete an application form 
  2. Attend a free 1 hour consultation to be eligible for selection

For more ​information and to apply, please contact:

Rachel Salsman
1-800-263-3463 ext. 7262

A Nuclear Attack on Thrombosis and Inflammation

What is your doctor doing with this to stop your arterial inflammation? ANYTHING AT ALL? 
  1. Edward M. Conway
+ Author Affiliations
  1. From the Department of Medicine, Centre for Blood Research, University of British Columbia, Vancouver, Canada.
  1. Correspondence to Edward M. Conway, MD, PhD, Department of Medicine, Centre for Blood Research, 4306-2350 Health Sciences Mall, University of British Columbia, Vancouver BC V6T 1Z3, Canada. E-mail  
Email for your doctor if they have questions on the procedures. There are no excuses for your doctor not applying this for you.
Key Words:
Thrombomodulin is a transmembrane glycoprotein expressed on the lumenal surface of endothelial cells, where it maintains vascular homeostasis via its anti-inflammatory, anticoagulant, and anti-fibrinolytic properties. These effects of thrombomodulin are achieved through dynamic interactions primarily with thrombin, protein C, thrombin activatable fibrinolysis inhibitor, complement components, and the proinflammatory danger signal high mobility group box 1 (HMGB1).1 When bound to thrombomodulin, thrombin loses its procoagulant/proinflammatory properties, while efficiently generating activated protein C and activated thrombin activatable fibrinolysis inhibitor. Activated protein C is a potent anticoagulant, anti-inflammatory and cytoprotective protease. Activated thrombin activatable fibrinolysis inhibitor inhibits fibrinolysis, and inactivates proinflammatory mediators and anaphylatoxins. The lectin-like domain of thrombomodulin also dampens inflammation by blocking HMGB1 and suppressing complement activation. Diminished expression of thrombomodulin is a feature of endothelial cell dysfunction, and it is a driver in the pathogenesis of several disorders, including venous thromboembolic disease, sepsis, disseminated intravascular coagulation (DIC), atherosclerosis, stroke, inflammatory arthritis and colitis, thrombotic microangiopathies, and diabetic nephropathy. To offset the imbalance associated with reduced thrombomodulin, and with the aim of preventing organ damage, systemic administration of recombinant forms of thrombomodulin has shown efficacy in several preclinical models of thrombosis and inflammation, and in humans with DIC and sepsis.2
See accompanying article on page 361
Yang et al3 have taken a different approach to augment endothelial thrombomodulin and limit disease, particularly focusing on thrombosis. Going nuclear, they examined the role of 2 transcription factors, Nur77 and Nor1, members of the family of nuclear orphan NR4A receptors. These …

Systems Biology and Noninvasive Imaging of Atherosclerosis

I couldn't tell at all from this limited part of the article what to ask my doctor to do to image my arteries to see what risks I have.
  1. Zahi A. Fayad
+ Author Affiliations
  1. From the Translational and Molecular Imaging Institute, Icahn School of Medicine at Mount Sinai, New York, NY (C.C., W.J.M.M., Z.A.F.); Department of Medical Biochemistry, Academic Medical Center, Amsterdam, The Netherlands (W.J.M.M.); and Center for Systems Biology, Massachusetts General Hospital, Harvard Medical School, Boston, MA (M.N.).
  1. Correspondence to Claudia Calcagno, MD, PhD, Translational and Molecular Imaging Institute, Icahn School of Medicine at Mount Sinai, New York, NY 10029. E-mail
Key Words:
Atherosclerosis is a systemic disease of the arterial vessel wall. Although the mortality due to cardiovascular events is decreasing, the prevalence of atherosclerosis and its comorbidities, and the consequent heath care costs are expected to rise sharply in the near future.1
Because the precise cause and pathogenesis of this complex, multifactorial disease are still not fully understood, the clinical assessment of cardiovascular risk has been traditionally based on population risk factors (RFs).2 However, this approach still largely fails to capture the individual’s cardiovascular risk: most cardiovascular events occur in patients with 1 or few traditional RFs, whereas individuals classified as high risk may never experience clinical events.3
The past 10 years have seen a significant paradigm shift in our understanding of the mechanisms of atherogenesis. From being considered the mere result of passive lipid accumulation in the vessel wall, atherosclerosis is now classified as an active inflammatory condition.4,5 The presence of abundant, active inflammatory cells is a known hallmark of high risk, vulnerable atherosclerotic plaques.4,5 Many studies have identified several systemic proinflammatory conditions (such as lupus,6 rheumatoid arthritis,79 and primary cardiovascular events themselves10) as emerging, independent RFs for atherosclerosis. New evidence suggests that atherosclerosis arises from the complex influence of genetic, environmental, and behavioral variables on systemic and local inflammation through a complex network of molecules, cells, and organs. 
Thanks to the recent technological advancements of high-throughput ‘-omics’, a plethora of the genes, proteins, and cells …

Motor System Reorganization After Stroke: Stimulating and Training Toward Perfection

No point in you asking about this because your doctor will already have applied everything in here to your stroke protocols. You know how current and up-to-date your doctor is.


Stroke instigates regenerative responses that reorganize connectivity patterns among surviving neurons. The new connectivity patterns can be suboptimal for behavioral function. This review summarizes current knowledge on post-stroke motor system reorganization and emerging strategies for shaping it with manipulations of behavior and cortical activity to improve functional outcome.
©2015 Int. Union Physiol. Sci./Am. Physiol. Soc.
[PubMed - in process]

[Available on 2016-09-01]

Mechanisms and Functional Significance of Stroke-Induced Neurogenesis

No point in you reading this because your doctor will already have applied everything in here to your stroke protocols.
Pages and pages of references supporting this that your doctor will also be conversant in. Don't bother asking any questions about points in here, that would be questioning your doctors' competence. You would hate to hurt their fee fees.

  • GIGA-Neurosciences, University of Liege, C.H.U. Sart Tilman, Liege, 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.


Stroke is the second leading cause of death, the most common cause of adult-acquired disability and affects one in every six people worldwide (Moskowitz et al., 2010). The number of people who survive a stroke is increasing, and with an aging population, the incidence and prevalence of stroke are predicted to rise even more (Sun et al., 2012). Despite years of research, effective treatments remain elusive. Currently, the only proven therapy for acute ischemic stroke is systemic thrombolysis with recombinant tissue plasminogen activator (rtPA). To be effective, rtPA must be administered within a maximum of 4.5 h after the symptoms first start. This short timeframe and potential adverse effects have limited the use of rtPA to 3–5% of stroke patients (Ruan et al., 2015). Grafting stem cells represents a compelling alternative and offers both a wide array and an unlimited supply of cells. Indeed, the transplantation of neural stem cells (NSCs), mesenchymal stem cells (MSCs), embryonic stem cells (ESCs), or induced pluripotent stem cells (iPSCs) could be used to replace neuronal loss after stroke (Kalladka and Muir, 2014). However, exogenous stem cell therapy has both technical and ethical issues. For instance, cell survival and migration rely heavily on the timing and mode of delivery (Li et al., 2010; Darsalia et al., 2011). Moreover, surgical procedure and toxicity (as cancer induction) increase the complexity of transplanted cell therapies (Kawai et al., 2010; Ben-David and Benvenisty, 2011). Finally, some ethical issues may arise from the use of fetal/embryonic cells.
Despite the fact that the central nervous system (CNS) has a limited repair capacity (Nakagomi et al., 2011), some degree of spontaneous recovery from brain ischemia invariably occurs (Yu et al., 2014). This repair process involves neurogenesis, angiogenesis, and axonal sprouting and synaptogenesis. Here we concentrate on the events that are associated with the production of new neurons and not the mechanisms that involve the reorganization of connectivity among surviving neurons, which is reviewed elsewhere (Jones and Adkins, 2015).
Recent experimental findings have raised the possibility that functional improvement after stroke may be induced through neuronal replacement by endogenous NSCs. Indeed, the original dogma that no new neurons are formed after birth has been definitively overturned during the past few decades. The discovery of the thymidine analog bromodeoxyuridine (BrdU)—that incorporates into DNA in S-phase and can be detected by immunohistochemistry—has allowed researchers to conclusively demonstrate the generation of new neurons in the brain of all adult mammals including humans (Eriksson et al., 1998; Gage, 2000). This production of new neurons in the adult brain—so-called adult neurogenesis—takes place in areas called neurogenic niches. The subventricular zone (SVZ) of the lateral ventricle and the subgranular zone (SGZ) of the dentate gyrus (DG) are the two main neurogenic niches containing adult NSCs that proliferate, divide and differentiate into mature neurons. Recently, new evidence have highlighted that adult neurogenesis could also takes place in other brain areas, along the ventricular system, mostly in pathological conditions (Lin and Iacovitti, 2015).
The capacity to produce new neurons in the adult brain and the ability of the ischemia-injured adult brain to partially recover suggest a possible relationship between adult neurogenesis and stroke recovery. Indeed, many studies have shown an increase in cell proliferation in the rodent SVZ following ischemic injury (Thored et al., 2006), and evidence for stroke-induced neurogenesis in the human brain has also been reported (Jin et al., 2006). In addition, endogenous brain repair is not limited to neurogenic niches. Recent studies have shown that glial cells surrounding the infarct core can be reactivated following ischemia. Indeed, pericytes, oligodendrocyte precursors, and astrocytes are all able to differentiate into neurons following brain injury (Robel et al., 2011; Heinrich et al., 2014; Nakagomi et al., 2015; Torper et al., 2015). Moreover, surviving neurons may reorganize their connections in a manner that supports some degree of spontaneous improvement. Therefore, a promising field of investigation is focused on triggering and stimulating this self-repair system to replace dead neurons following an ischemic attack.

Arrhythmia and Electrophysiology Consumption of Caffeinated Products and Cardiac Ectopy

But did they consider those studies that 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.  Sometimes I wonder if anyone in stroke has a thinking cap or is it tin foil.

Arrhythmia and Electrophysiology Consumption of Caffeinated Products and Cardiac Ectopy

  1. Gregory M. Marcus, MD, MAS1
+ Author Affiliations
  1. 1University of California, San Francisco, San Francisco, CA (S.D., J.W.D., E.V., G.M.M.)
  2. 2Washington University School of Medicine, St. Louis, MO (P.K.S.)
  3. 3Knight Cardiovascular Institute, Oregon Health & Science University, Portland, OR (T.A.D.)
  4. 4University of Washington and Group Health Research Institute, Seattle, WA (S.R.H.)
  1. Correspondence to:
    Gregory M. Marcus, MD, MAS, 505 Parnassus Ave, M‐1180B, Box 0124, San Francisco, CA 94143‐0124. E‐mail:
  • Received August 5, 2015.
  • Accepted December 3, 2015.
This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.


Background Premature cardiac contractions are associated with increased morbidity and mortality. Though experts associate premature atrial contractions (PACs) and premature ventricular contractions (PVCs) with caffeine, there are no data to support this relationship in the general population. As certain caffeinated products may have cardiovascular benefits, recommendations against them may be detrimental.
Methods and Results We studied Cardiovascular Health Study participants with a baseline food frequency assessment, 24‐hour ambulatory electrocardiography (Holter) monitoring, and without persistent atrial fibrillation. Frequencies of habitual coffee, tea, and chocolate consumption were assessed using a picture‐sort food frequency survey. The main outcomes were PACs/h and PVCs/hour. Among 1388 participants (46% male, mean age 72 years), 840 (61%) consumed ≥1 caffeinated product per day. The median numbers of PACs and PVCs/h and interquartile ranges were 3 (1–12) and 1 (0–7), respectively. There were no differences in the number of PACs or PVCs/h across levels of coffee, tea, and chocolate consumption. After adjustment for potential confounders, more frequent consumption of these products was not associated with ectopy. In examining combined dietary intake of coffee, tea, and chocolate as a continuous measure, no relationships were observed after multivariable adjustment: 0.48% fewer PACs/h (95% CI −4.60 to 3.64) and 2.87% fewer PVCs/h (95% CI −8.18 to 2.43) per 1‐serving/week increase in consumption.
Conclusions In the largest study to evaluate dietary patterns and quantify cardiac ectopy using 24‐hour Holter monitoring, we found no relationship between chronic consumption of caffeinated products and ectopy.


Premature cardiac contractions, otherwise known as atrial and ventricular ectopy, are common throughout the general population.12 Previously, these ectopic beats were believed to be harmless in the absence of known cardiovascular disease or symptoms; however, there is now evidence to indicate that premature atrial contractions (PACs) and premature ventricular contractions (PVCs) are associated with increased cardiovascular morbidity and mortality. PACs are known to initiate paroxysms of atrial fibrillation (AF), and targeted ablation of ectopic foci in the atria can eliminate or significantly reduce AF recurrence.3 In addition, we previously showed that the PAC count is a particularly useful predictor of incident AF in older adults,4 and others have demonstrated that increased PACs in apparently healthy individuals are associated with incident AF, stroke, and death.5 With regard to PVCs, the presence of even one PVC during a 2‐minute ECG has been associated with an increased risk of incident congestive heart failure (CHF), coronary artery disease (CAD) events, and CAD‐related death.67 Additionally, our group has previously demonstrated that a higher frequency of PVCs is associated with an increase in incident CHF and with increased mortality.8 Furthermore, recent evidence from the electrophysiology laboratory has shown that eradication of PVCs via radiofrequency ablation among patients with idiopathic systolic heart failure can normalize ventricular function, suggesting that PVCs alone are sufficient to result in heart failure.9

More at link