Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 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:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. 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 lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Tuesday, June 24, 2014

Cocoa Extract May Counter Specific Mechanisms of Alzheimer’s Disease

Is this something your doctor should be setting up a protocol for preventing your 33% dementia chance post-stroke from an Australian study?
This may explain these reports:

Could Hot Cocoa Improve Brainpower in Seniors?

Cocoa, Blood Flow and the Brain

Hot Cocoa May Boost Seniors' Brain Power

Eating small bar of chocolate cuts risks of stroke in men

http://www.alphagalileo.org/ViewItem.aspx?ItemId=143050&CultureCode=en
A specific preparation of cocoa-extract called Lavado may reduce damage to nerve pathways seen in Alzheimer’s disease patients’ brains long before they develop symptoms, according to a study conducted at the Icahn School of Medicine at Mount Sinai and published June 20 in the Journal of Alzheimer’s Disease (JAD). 
Specifically, the study results, using mice genetically engineered to mimic Alzheimer’s disease, suggest that Lavado cocoa extract prevents the protein β-amyloid- (Ab) from gradually forming sticky clumps in the brain, which are known to damage nerve cells as Alzheimer’s disease progresses.
Lavado cocoa is primarily composed of polyphenols, antioxidants also found in fruits and vegetables, with past studies suggesting that they prevent degenerative diseases of the brain.
The Mount Sinai study results revolve around synapses, the gaps between nerve cells. Within healthy nerve pathways, each nerve cell sends an electric pulse down itself until it reaches a synapse where it triggers the release of chemicals called neurotransmitters that float across the gap and cause the downstream nerve cell to “fire” and pass on the message.
The disease-causing formation of Aβ oligomers – groups of molecules loosely attracted to each other –build up around synapses. The theory is that these sticky clumps physically interfere with synaptic structures and disrupt mechanisms that maintain memory circuits’ fitness. In addition, Aβ triggers immune inflammatory responses, like an infection, bringing an on a rush of chemicals and cells meant to destroy invaders but that damage our own cells instead.
“Our data suggest that Lavado cocoa extract prevents the abnormal formation of Aβ into clumped oligomeric structures, to prevent synaptic insult and eventually cognitive decline,” says lead investigator Giulio Maria Pasinetti, MD, PhD, Saunders Family Chair and Professor of Neurology at the Icahn School of Medicine at Mount Sinai.  “Given that cognitive decline in Alzheimer’s disease is thought to start decades before symptoms appear, we believe our results have broad implications for the prevention of Alzheimer’s disease and dementia.
Evidence in the current study is the first to suggest that adequate quantities of specific cocoa polyphenols in the diet over time may prevent the glomming together of Aβ into oligomers that damage the brain, as a means to prevent Alzheimer’s disease.
The research team led by Dr. Pasinetti tested the effects of extracts from Dutched, Natural, and Lavado cocoa, which contain different levels of polyphenols.  Each cocoa type was evaluated for its ability to reduce the formation of Ab oligomers and to rescue synaptic function.  Lavado extract, which has the highest polyphenol content and anti-inflammatory activity among the three, was also the most effective in both reducing formation of Ab oligomers and reversing damage to synapses in the study mice.
“There have been some inconsistencies in medical literature regarding the potential benefit of cocoa polyphenols on cognitive function,” says Dr. Pasinetti.  “Our finding of protection against synaptic deficits by Lavado cocoa extract, but not Dutched cocoa extract, strongly suggests that polyphenols are the active component that rescue synaptic transmission, since much of the polyphenol content is lost by the high alkalinity in the Dutching process.”
Because loss of synaptic function may have a greater role in memory loss than the loss of nerve cells, rescue of synaptic function may serve as a more reliable target for an effective Alzheimer’s disease drug, said Dr. Pasinetti.
The new study provides experimental evidence that Lavado cocoa extract may influence Alzheimer’s disease mechanisms by modifying the physical structure of Ab oligomers.  It also strongly supports further studies to identify the metabolites of Lavado cocoa extract that are active in the brain and identify potential drug targets.
In addition, turning cocoa-based Lavado into a dietary supplement may provide a safe, inexpensive and easily accessible means to prevent Alzheimer’s disease, even in its earliest, asymptomatic stages.
Researchers from Kanazawa University in Japan contributed to the study and the cocoa used in the study was a gift from Dr. Jeffrey Hurst of the Hershey Company.

Not even cell death can stop the alarm

This might explain some of the neuronal cascade of death. So whom is working on this?
http://www.alphagalileo.org/ViewItem.aspx?ItemId=143009&CultureCode=en
Even after a cell dies, components of the immune system remain active and continue to fuel inflammatory reactions. An international team of researchers under the direction of scientists from the Institute of Innate Immunity at the University Hospital of Bonn has discovered how this incredible form of communication works. The findings offer potentially novel approaches for therapies against many serious diseases that affect a large part of the population, such as gout, atherosclerosis and Alzheimer's disease. The exciting new results are now published in the renowned journal "Nature Immunology".
When there is stress in living immune cells, – for example due to the detection of microbes, or the deposition of uric acid crystals in joints, cholesterol in blood vessels or Alzheimer's plaques in the brain – the so-called ‘inflammasome’ sounds the alarm. Inflammasomes are large multiprotein complexes, which form when they sense cell stress. The inflammasomes activate an enzyme, which stimulates important messengers that in turn trigger an inflammatory reaction. During this cell activation, the affected immune cells die and thus the inflammatory reaction should come to a halt. "This mechanism primarily protects the body from infections and harmful influences," says Prof. Eicke Latz, the director of the Institute of Innate Immunity at the University Hospital in Bonn.
Strikingly, these new findings reveal that inflammasomes remain active even when the cells have died. The scientists were able to demonstrate that activated inflammasomes also have enzymatic functions outside of the living cell and can thus activate additional messengers. In a type of chain reaction, the inflammasomes released from dying cells are taken up by neighboring immune cells where they can activate more inflammasomes. This discovery was made by an international team of researchers under the direction of the members from the Institute of Innate Immunity, together with scientists from Hannover Medical School, the University of Massachusetts Medical School (USA), the German Center for Neurodegenerative Diseases (DZNE) in Bonn, the University of Trondheim (Norway), the University of Newcastle (Australia) and the Zurich University Hospital (Switzerland).
Protein complexes shift into defense mode
When the inflammasomes are switched on, within seconds they form functional protein complexes, which can be as large as a bacterium. "In the event of stress or infection, this protein complex forms and provokes the activation of pro-inflammatory messengers within the cell and – as we now know – this can also occur outside of the cell. In this way, there can be a very rapid inflammatory reaction which helps the undesired insult or microbial invaders to be eliminated as quickly as possible," explains lead author Dr. Bernardo S. Franklin, a fellow of the Alexander von Humboldt Foundation working in Prof. Latz's team.
Using fluorescence techniques, the researchers labeled the inflammasome in immune cells. Whenever it was active, it formed a fluorescent protein complex, reminiscent of small stars glowing inside the cell. Using this method, the scientists were able to track the inflammasome after cell death, and show that it remained switched on as an intact protein complex. They also found that once released from the dead cell, it stimulated neighboring cells to undergo an inflammatory reaction. Furthermore, they found that these extracellular complexes accumulate in the lungs of patients with chronic lung disease.
Starting points for new therapies against widespread diseases
"Normally, the immune system is very helpful for averting harmful damage to tissue by initiating an inflammatory reaction," says Prof. Latz.  However, if such inflammatory reactions are excessive or if they persist for longer than necessary, this may contribute to common diseases of Western society, such as gout, Alzheimer's disease, diabetes or atherosclerosis. With the discovery of extracellular inflammasomes, the researchers have revealed an interesting avenue for potential new therapies: "If we are able to produce suitable antibodies, it is likely we could contain the alarm of the inflammasome outside of cells and thus keep harmful chronic inflammatory reactions at bay, without affecting the necessary response inside the cell" says Prof. Latz.


Newman's Notes: tPA -- Get With the Evidence

All this brainpower and not one understands that delivering tPA faster is not the solution to reduced disability. Damn it all tPA has only a 12% efficacy and does nothing on stopping the neuronal cascade of death. This is so f*cking simple to prove. You do daily MRI scans to see the progression of the dead area during the first week. And maybe then these idiots will solve the correct problem.
tPA delivery times are not the problem to solve. Reducing neuronal cell death is the problem to solve.
http://www.medpagetoday.com/Neurology/Strokes/46455?
The last paragraphs here;
The outcomes in stroke patients -- even those who don't get thrombolytics and, in fact, mostly in those who don't get thrombolytics -- have improved. Outcomes have improved immensely for almost every group over the last 10 to 12 years.
When you look at 2003 to 2010, we know that stroke mortality has been going down. We know it's been going down, partly because of epidemiologic trends that preceded the advent of the drug, and partly because of high quality stroke unit care. There is no reason to believe that these improvements have had anything to do with thrombolytics.
So, it's a little bit strange to see the JAMA trumpeting this as a success and talking about it in ways both in an editorial and in the discussion sections of this study, that suggest thrombolytic administration minutes earlier is the reason that stroke mortality went down.
The two almost certainly have nothing to do with each other.
This is probably, and sadly, another example of wishful thinking. We would like to believe that thrombolytics could save lives but randomized trials strongly contradict the idea. But we wish it was true, just like we wish that getting the drugs on board earlier could improve outcomes.
In the end, judging from the one marker that thrombolytics are supposed to affect -- disability -- the drugs seem to have failed yet again.

Read the rest and weep because our doctors still have absolutely no idea on how to treat stroke.



New iLimb arms and hands are smarter and more subtle prosthetics

With just a little bit of additional innovation I'm sure this could be repurposed for survivors. But that would require a stroke survivors advocate with enough clout and brains to convince the company to move in that direction.  I'm positive our stroke associations have no such person and don't even realize the possibilities.
And that market could be hundreds of thousands of people in the US, millions in the world.
http://medcitynews.com/2014/06/touch-bionics-makes-six-million-dollar-man-reality/?

Converge - SUMMIT FOR HEALTHCARE INNOVATION July 15-16, 2014, Philadelphia

You will notice that there is no attempt to include patients at all. This is where ePatient Dave belongs.
I bet these people never talk to patients at all.
Failure, failure, failure.
http://events.medcitynews.com/converge/

Monday, June 23, 2014

Memantine Enhances Recovery From Stroke

And why the f*ck won't your doctor try this after your stroke? I bet any patient would agree to signing the release form. If my doctor had any brains at all he could have asked me to allow immediate administration of statins even though testing had only been proven in rats 3 years prior.
If you want something like this you are going to have to scream at your doctors because they will never try something new that might save a whole slew of your neurons. And what the hell are you paying them for? To sit around and watch your neurons die in the neuronal cascade of death?
http://stroke.ahajournals.org/content/45/7/2093.abstract?etoc
  1. Correspondence to Kevin C. Brennan, MD, 383 Colorow Dr, Room 364, Salt Lake City, UT 84103. E-mail k.c.brennan@hsc.utah.edu.
  1. * Drs López-Valdés and Clarkson contributed equally.

Abstract

Background and Purpose—Stroke treatment is constrained by limited treatment windows and the clinical inefficacy of agents that showed preclinical promise. Yet animal and clinical data suggest considerable poststroke plasticity, which could allow treatment with recovery-modulating agents. Memantine is a well-tolerated N-methyl-D-aspartate glutamate receptor antagonist in common use for Alzheimer disease.
Methods—Memantine, 30 mg/kg per day, or vehicle, was delivered chronically in drinking water beginning >2 hours after photothrombotic stroke.
Results—Although there was no difference in infarct size, behavior, or optical intrinsic signal maps in the first 7 days after stroke, mice treated chronically with memantine showed significant improvements in motor control, measured by cylinder test and grid-walking performance, compared with vehicle-treated animals. Optical intrinsic signal revealed an increased area of forepaw sensory maps at 28 days after stroke. There was decreased reactive astrogliosis and increased vascular density around the infarcted cortex. Peri-infarct Western blots revealed increased brain-derived neurotrophic factor and phosphorylated-tropomyosin–related kinase-B receptor expression.
Conclusions—Our results suggest that memantine improves stroke outcomes in an apparently non-neuroprotective manner involving increased brain-derived neurotrophic factor signaling, reduced reactive astrogliosis, and improved vascularization, associated with improved recovery of sensory and motor cortical function. The clinical availability and tolerability of memantine make it an attractive candidate for clinical translation.

Six-Minute Magnetic Resonance Imaging Protocol for Evaluation of Acute Ischemic Stroke

So what. This will be obsolete soon.  Because of these;
Maybe when we get actual objective diagnosis when these come online:
1. Star Trek-style 'tricorder' invention offered $10m prize
2. Strokefinder quickly differentiates bleeding strokes from clot-induced strokes
3.  One of these 17 ways still need to be be proven for fast and objective diagnosis.

Six minute MRI here:
http://stroke.ahajournals.org/content/45/7/1985.abstract?etoc

Pushing the Boundaries

  1. Chelsea S. Kidwell, MD
+ Author Affiliations
  1. From the Departments of Medical Imaging (K.N., R.K., G.C., A.M., C.S.K.) and Neurology (J.T., K.D., B.M.C., C.S.K.), University of Arizona, Tucson; and Department of Radiological Sciences, University of California, Los Angeles (P.V.).
  1. Correspondence to Kambiz Nael, MD, Neuroradiology Section, Department of Medical Imaging, University of Arizona Medical Center, 1501 N Campbell, PO Box 245067, Tucson, AZ 85724. E-mail kambiznael@gmail.com

Abstract

Background and Purpose—If magnetic resonance imaging (MRI) is to compete with computed tomography for evaluation of patients with acute ischemic stroke, there is a need for further improvements in acquisition speed.
Methods—Inclusion criteria for this prospective, single institutional study were symptoms of acute ischemic stroke within 24 hours onset, National Institutes of Health Stroke Scale ≥3, and absence of MRI contraindications. A combination of echo-planar imaging (EPI) and a parallel acquisition technique were used on a 3T magnetic resonance (MR) scanner to accelerate the acquisition time. Image analysis was performed independently by 2 neuroradiologists.
Results—A total of 62 patients met inclusion criteria. A repeat MRI scan was performed in 22 patients resulting in a total of 84 MRIs available for analysis. Diagnostic image quality was achieved in 100% of diffusion-weighted imaging, 100% EPI-fluid attenuation inversion recovery imaging, 98% EPI-gradient recalled echo, 90% neck MR angiography and 96% of brain MR angiography, and 94% of dynamic susceptibility contrast perfusion scans with interobserver agreements (k) ranging from 0.64 to 0.84. Fifty-nine patients (95%) had acute infarction. There was good interobserver agreement for EPI-fluid attenuation inversion recovery imaging findings (k=0.78; 95% confidence interval, 0.66–0.87) and for detection of mismatch classification using dynamic susceptibility contrast-Tmax (k=0.92; 95% confidence interval, 0.87–0.94). Thirteen acute intracranial hemorrhages were detected on EPI-gradient recalled echo by both observers. A total of 68 and 72 segmental arterial stenoses were detected on contrast-enhanced MR angiography of the neck and brain with k=0.93, 95% confidence interval, 0.84 to 0.96 and 0.87, 95% confidence interval, 0.80 to 0.90, respectively.
Conclusions—A 6-minute multimodal MR protocol with good diagnostic quality is feasible for the evaluation of patients with acute ischemic stroke and can result in significant reduction in scan time rivaling that of the multimodal computed tomographic protocol.

9th World Stroke Congress in Istanbul, October 22-25, 2014

I'm sure nothing useful for survivors will come out of this. But its a vacation and your hospital is paying for your neurologists to attend.
http://www2.kenes.com/stroke2014/info/Pages/WelcomeLetter.aspx
Look at this pathetic list of topics from 2012. Not a single one on rehab, protocols or cascade of death.
Big f*cking whoopee.
WSC 2012 topics included:
  • Acute Stroke Management
  • Acute Reperfusion Treatment
  • Acute Stroke: new treatments concepts
  • Acute Neuroimaging
  • Neurocritical Management
  • Hemorrhage – Intraparenchymal
  • Aneurysm and Vascular Malformations
  • Venous diseases
  • TIA and minor Stroke
  • Cerebrovascular Occlusive Disease
  • Heart and Brain
  • Infections Diseases and Stroke
  • Vascular Cognitive Impairment/ Vascular Dementia
  • Uncommon Stroke Disorders
  • Experimental and Translational Neuroscience
  • Genetics
  • Epidemiology of stroke
  • Pediatric Stroke
  • Preventive Stroke Strategies
  • Diagnosis
  • Large Clinical Trials
  • On-going Clinical Trials
  • Outcomes and Quality of Care
  • Stroke Care Systems
  • Stroke Support Organisation
  • Multidisciplinary Clinical Rehabilitation
  • Public Awareness/Advocacy
  • Nursing
  • Fruits and vegetables consumption and risk of stroke

    And I wonder if the whole decrease in stroke is caused by the potassium in bananas?    Potassium 21%   Why eat three bananas a day?

    Do the authors not know about bananas?


    Fruits and vegetables consumption and risk of stroke

     The authors conducted a meta–analysis to summarize evidence from prospective cohort studies about the association of fruits and vegetables consumption with the risk of stroke. Fruits and vegetables consumption are inversely associated with the risk of stroke.
    Methods
    • Pertinent studies were identified by a search of Embase and PubMed databases to January 2014.
    • Study–specific relative risks with 95% confidence intervals were pooled using a random–effects model.
    • Dose–response relationship was assessed by restricted cubic spline.
    Results
    • Twenty prospective cohort studies were included, involving 16 981 stroke events among 760629 participants.
    • The multivariable relative risk (95% confidence intervals) of stroke for the highest versus lowest category of total fruits and vegetables consumption was 0.79 (0.75–0.84), and the effect was 0.77 (0.71–0.84) for fruits consumption and 0.86 (0.79–0.93) for vegetables consumption.
    • Subgroup and meta–regression showed that the inverse association of total fruits and vegetables consumption with the risk of stroke was consistent in subgroup analysis.
    • Citrus fruits, apples/pears, and leafy vegetables might contribute to the protection.
    • The linear dose–response relationship showed that the risk of stroke decreased by 32% (0.68 [0.56–0.82]) and 11% (0.89 [0.81–0.98]) for every 200 g per day increment in fruits consumption (P for nonlinearity=0.77) and vegetables consumption (P for nonlinearity=0.62), respectively.

    Researchers Find Gene Critical for Development of Brain Motor Center

    Well this is so simple, you follow this research to its natural conclusion. How can we use this to redevelop dead and damaged brains from stroke?
    http://www.biosciencetechnology.com/news/2014/06/researchers-find-gene-critical-development-brain-motor-center?
    In a report published in Nature Communications, an Ottawa-led team of researchers describe the role of a specific gene, called Snf2h, in the development of the cerebellum. Snf2h is required for the proper development of a healthy cerebellum, a master control centre in the brain for balance, fine motor control and complex physical movements.
    Athletes and artists perform their extraordinary feats relying on the cerebellum. As well, the cerebellum is critical for the everyday tasks and activities that we perform, such as walking, eating and driving a car. By removing Snf2h, researchers found that the cerebellum was smaller than normal, and balance and refined movements were compromised.
    Led by Dr. David Picketts, a senior scientist at the Ottawa Hospital Research Institute and professor in the Faculty of Medicine at the University of Ottawa, the team describes the Snf2h gene, which is found in our brain's neural stem cells and functions as a master regulator. When they removed this gene early on in a mouse's development, its cerebellum only grew to one-third the normal size. It also had difficulty walking, balancing and coordinating its movements, something called cerebellar ataxia that is a component of many neurodegenerative diseases.
    "As these cerebellar stem cells divide, on their journey toward becoming specialized neurons, this master gene is responsible for deciding which genes are turned on and which genes are packed tightly away," said Dr. Picketts. "Without Snf2h there to keep things organized, genes that should be packed away are left turned on, while other genes are not properly activated. This disorganization within the cell’s nucleus results in a neuron that doesn't perform very well—like a car running on five cylinders instead of six."
    The cerebellum contains roughly half the neurons found in the brain. It also develops in response to external stimuli. So, as we practice tasks, certain genes or groups of genes are turned on and off, which strengthens these circuits and helps to stabilize or perfect the task being undertaken. The researchers found that the Snf2h gene orchestrates this complex and ongoing process. These master genes, which adapt to external cues to adjust the genes they turn on and off, are known as epigenetic regulators.
    "These epigenetic regulators are known to affect memory, behaviour and learning," said Dr. Picketts. "Without Snf2h, not enough cerebellar neurons are produced, and the ones that are produced do not respond and adapt as well to external signals. They also show a progressively disorganized gene expression profile that results in cerebellar ataxia and the premature death of the animal."
    There are no studies showing a direct link between Snf2h mutations and diseases with cerebellar ataxia, but Dr. Picketts added that it "is certainly possible and an interesting avenue to explore."
    In 2012, Developmental Cell published a paper by Dr. Picketts' team showing that mice lacking the sister gene Snf2l were completely normal, but had larger brains, more cells in all areas of the brain and more actively dividing brain stem cells. The balance between Snf2l and Snf2h gene activity is necessary for controlling brain size and for establishing the proper gene expression profiles that underlie the function of neurons in different regions, including the cerebellum.
    This research was funded by the Canadian Institutes of Health Research and the U.S. National Institutes of Health.

    Wheatgrass extract aids stroke recovery in hemiplegic patient

    Miracles are occurring, notify the Nobel committee. This would be an extremely cheap solution to all your stroke problems.

    Wheatgrass extract aids stroke recovery in hemiplegic patient

    Behavioral and Neural Correlates of Executive Functioning in Musicians and Non-Musicians

    Have your doctor identify whether this means that musically trained people have a larger cognitive reserve. And can that reserve be used to handle brain insults like stroke and dementia? What age should training start? And for how long? Can you pick this up mid-life?
    http://www.plosone.org/article/info:doi/10.1371/journal.pone.0099868
    • Jennifer Zuk,
    • Christopher Benjamin,
    • Arnold Kenyon,
    • Nadine Gaab mail

    • Published: June 17, 2014
    • DOI: 10.1371/journal.pone.0099868

    Abstract

    Executive functions (EF) are cognitive capacities that allow for planned, controlled behavior and strongly correlate with academic abilities. Several extracurricular activities have been shown to improve EF, however, the relationship between musical training and EF remains unclear due to methodological limitations in previous studies. To explore this further, two experiments were performed; one with 30 adults with and without musical training and one with 27 musically trained and untrained children (matched for general cognitive abilities and socioeconomic variables) with a standardized EF battery. Furthermore, the neural correlates of EF skills in musically trained and untrained children were investigated using fMRI. Adult musicians compared to non-musicians showed enhanced performance on measures of cognitive flexibility, working memory, and verbal fluency. Musically trained children showed enhanced performance on measures of verbal fluency and processing speed, and significantly greater activation in pre-SMA/SMA and right VLPFC during rule representation and task-switching compared to musically untrained children. Overall, musicians show enhanced performance on several constructs of EF, and musically trained children further show heightened brain activation in traditional EF regions during task-switching. These results support the working hypothesis that musical training may promote the development and maintenance of certain EF skills, which could mediate the previously reported links between musical training and enhanced cognitive skills and academic achievement.


    Sunday, June 22, 2014

    mosquitos and trail clearing

    This year I'm going out every chance I get because there are still lots of branches and trees over the trails. It requires long sleeved shirts and mosquito spray to keep the nasty critters away. Applying the pump spray to my good hand and arm doesn't work since my left hand has no useful functionality yet. So I spray my left hand with a bit extra and rub the back of my right hand over it.  Smoking cigars doesn't really keep the mosquitos away from the face. I'm going to have to use the mosquito head net. The water in the woods has receded enough that I can at least walk though with my Wellies. I had to buy a boot jack to get them off. One handed removal of Wellies with my high instep is well nigh impossible.

    Alcohol and CVD: The Tippling Point

    A full discussion on it here: You will need to register to Medscape to read it.
    http://www.medscape.com/viewarticle/826979?src=wnl_edit_specol&uac=107573PV
    I'm sure your doctor will reflexively say no without any supporting documentation.

    My documentation is here; but you know better than to listen to anything I have to say. I'm brain-damaged and obviously know nothing.
    Both pros and cons in these;

    Drinking alcohol several times a week increases the risk of stroke mortality

    Alcohol could have cognitive benefits – depending on your genes

    No Amount of Alcohol Is Safe

    Chase your stroke recovery by drinking

    Alcohol intake and risk of stroke: A dose-response meta-analysis of prospective studies

    Acute effects of beer on endothelial function and hemodynamics: A single-blind, crossover study in healthy volunteers

    Hangovers increase risk of stroke in men

    Smarter People Tend To Drink More Alcohol

    Pub trip helps Tredworth stroke victim recover 

    One Drink With Alcohol Immediately Doubles Stroke Risk

    Alcohol intake in the elderly affects risk of cognitive decline and dementia

     

     

     

     

     

     

     

     

     

    'Research' on coffee vs. tea

    This is great, more proof than coffee makes you live longer. And does your doctor know about this?
    King Gustaf III’s coffee-kills-which-murderous-twin experiment

    http://www.improbable.com/2014/06/22/king-gustaf-iiis-coffee-kills-which-murderous-twin-experiment
    “Coffee drinking was compared with tea drinking in monozygotic twins in 18th century,” Lars Breimer, BMJ, vol. 312, June 15, 1996, p. 1539. The author, at the Royal Free Hospital School of Medicine in London, explains:

        “One of the more peculiar attempts to throw light on the question of whether drinking coffee is bad for one’s health’ was carried out in the 18th century by King Gustaf III of Sweden…. A pair of monozygotic twins had been sentenced to death for murder. Gustaf III commuted their death sentences to life imprisonment on the condition that one twin drank a large bowl of tea three times a day and that the other twin drank coffee. The twin who drank tea died first, aged 83-a remarkable age for the time. Thus the case was settled: coffee was the less dangerous of the two beverages. The king, on the other hand, was murdered at a masked ball in 1792 at the age of 45 and became the subject of an opera by Verdi.”

    Saturday, June 21, 2014

    Cast party after the Book of Mormon



    The cast party after the Book of Mormon. The guy we posed with was the guy looking to have sex with a baby because sex with virgins cured AIDs. Arnold convinced him that the Book of Mormon stated that sex with a frog would cure AIDs. Extremely irreverent and I'm sure quite insulting to Mormons, although they didn't cover the part about men ruling other planets after death.


    I hate the way my arm hangs, damnable spasticity, when walking it bangs into my crotch.

    Medical marijuana: New York moves to legalize it, but advocates not thrilled

    This is just f*cking stupid. There is no way stroke survivors can use this at all.  You'll have to get directly in their faces and ask what the hell they are going to do when their parents have a stroke. GAH!!! the total stupidity of legislators and Cuomo.
    http://news.yahoo.com/medical-marijuana-york-moves-legalize-advocates-not-thrilled-172103678.html

    All the reasons for it here:

    Medical Marijuana and Stroke

    New Approach to Funding Alzheimer’s Research Could Pay Off

    Do we have any stroke association that is innovative enough to use this approach for stroke?  Stroke has 7 million plus survivors in the US so there is even more of a need for this than Alzheimers. Or do we have to wait for that great stroke association to arise?
    What does your stroke board of directors have to say about that?
    http://www.biosciencetechnology.com/news/2014/06/new-approach-funding-alzheimer%E2%80%99s-research-c uld-pay?

    Thornhill woman’s “stroke selfie” goes viral

    The takeaway from this is that stroke diagnosis is a complete failure. What is the ASA, NSA and WSO doing about that?  It was the second attack in two days — the first time she was sent home after being treated for stress.
    Maybe when we get actual objective diagnosis when these come online:
    1. Star Trek-style 'tricorder' invention offered $10m prize
    2. Strokefinder quickly differentiates bleeding strokes from clot-induced strokes
    3.  One of these 17 ways still need to be be proven for fast and objective diagnosis.
    http://www.thestar.com/life/2014/06/20/thornhill_womans_stroke_selfie_goes_viral.html 
     

    Friday, June 20, 2014

    March of Dimes Canada, U of T sign deal to advance research in brain injuries, stroke

    If you are a member of the March of Dimes - Canada or know someone at the University of Toronto, you  need to contact them and ask very very specifically what their strategic plan is to address the problems in TBI and stroke. With no plan this is doomed to failure. And I bet no one associated with this is smart enough to understand their problem. With no plan they have just wasted 1.5 million Canadian.
    http://www.news-medical.net/news/20140619/March-of-Dimes-Canada-U-of-T-sign-deal-to-advance-research-in-brain-injuries-stroke.aspx

    $1.5 million donation establishes March of Dimes Canada Early Career Professorship

    Today, March of Dimes Canada and the University of Toronto (U of T) signed a $1.5 million agreement to advance research in recovery from brain injuries and stroke, making the donation to the University the largest made by the national charitable organization in its over 60 year history.
    Brain injuries and stroke affect 80,000 to 100,000 Canadians every year and are the leading cause of disability worldwide. Survivors often have difficulties with daily activities and participating in their communities due to mobility, communication, cognitive and perceptual impairments, and only about half are able to return to work. With this donation, March of Dimes Canada is acting on its mission to "maximize the independence, personal empowerment and community participation of people with physical disabilities" by establishing the March of Dimes Canada Early Career Professorship in U of T's Department of Occupational Science and Occupational Therapy.
    "This is the first major partnership we have with a university and we are excited at the prospect of working with the selected faculty member, with graduate students and with the wider university network to benefit Canadians with disabilities as it relates to our mission," said Andria Spindel, President and CEO of March of Dimes Canada.
    The March of Dimes Canada Early Career Professorship will provide a faculty member in the early stages of her or his research career with a well-established framework for investigating interventions and pathways to increase the independence and social integration of brain injury survivors. The professorship will also provide research evidence to enhance existing March of Dimes Canada programs, which serve more than 60,000 Canadians annually.
    "We are thrilled and proud to be the recipient of this landmark gift by March of Dimes Canada," says Dr. Susan Rappolt, Chair of U of T's Department of Occupational Science and Occupational Therapy. "This professorship creates tremendous capacity for new scientific evidence to improve the quality of life and productivity of individuals with acquired brain injuries and their families through new opportunities for training students and collaborating with our partners across the Rehabilitation Sector."
    The University of Toronto's rehabilitation scientists and practitioners work collaboratively to translate new research evidence into therapies that help individuals with brain injuries capitalize on their post-injury strengths to get them out of the hospital and back into their roles in their communities. The Department of Occupational Science and Occupational Therapy is an international leader in research on acquired brain injuries at the individual, community and societal levels.