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:

Thursday, December 31, 2015

Benefits of tPA Outweigh Risks in Ischemia Stroke, Even in Patients on Antiplatelet Medications

I wonder about the contraindication of tPA use in the last 3 months? I know I wasn't asked if I was taking aspirin or anything else.
Whom is going to decide if this is enough information to change the stroke protocol on this use? And then disseminate this to all stroke doctors, emergency rooms and stroke hospitals?
Our fucking failures of stroke associations obviously will not take on this challenge. You as a stroke patient are simply screwed. YOU will need to remember this and notify your emergency room doctors. Interview with:
Ying Xian, PhD

Assistant Professor of Medicine.
Member in the Duke Clinical Research Institute
Medical Research: What is the background for this study? What are the main findings?
Dr. Xian: Intravenous tissue plasminogen activator (tPA) is the only FDA approved medical therapy to reduce disability and improve outcomes for patients with acute ischemic stroke. But treatment with tPA also carries the risk of symptomatic intracranial hemorrhage (sICH), which is often fatal. Nearly half of ischemic stroke patients are taking antiplatelet drugs such as aspirin and/or clopidogrel prior to stroke. We found these patients had higher risk for sICH when treated with tPA. But the risk is relatively small. For every 147 patients on aspirin treated with tPA, only 1 more symptomatic intracranial hemorrhage as compared with those treated with tPA without prior antiplatelet therapy. The risk is slightly higher among those on dual antiplatelet therapy of aspirin and clopidogrel (number needed to harm 60). Despite the higher bleeding risk, patients treated with tPA on prior antiplatelet therapy appeared to have better functional outcomes in terms of ambulatory status and modified Rankin scale than those not on prior antiplatelet therapy. Therefore, overall the benefits of thrombolytic therapy may outweigh the risks.

Medical Research: What should clinicians and patients take away from your report?
Dr. Xian: Considering intravenous tPA is the only FDA approved medical therapy and remains substantially underused worldwide for patients with acute ischemic stroke, clinicians should consider intravenous tPA for eligible patients on prior antiplatelet therapy. I would like to quote from Dr. Mark Alberts, Vice Chair of Clinical Affairs in the Department of Neurology and Neurotherapeutics at UT Southwestern Medical Center, “the real risk is not treating.”
Medical Research: What recommendations do you have for future research as a result of this study?
Dr. Xian: As more potent P2Y12 inhibitors such as prasugrel and ticagrelor are increasingly used in the Unites States, future research is needed provide guidance on tPA for patients who developed ischemic stroke while taking these new antiplatelet drugs.

New rehab items from storage locker

Over Christmas I was back in Minnesota and picked up more stuff. Three sleeping bags, enough to allow me to go winter camping again as long as someone I trust can zip me up and out again. My backpack and a couple of Duluth Packs. My camping stove, Svea 123, the greatest stove I've owned. Now all I need is a tent.  My 16 inch gas powered chainsaw, trail clearing here I come. Several friends have said they would do interventions if I attempted to use that. Well I don't even listen to my own voice telling me not to do stuff.

Driving with the affected left arm

Don't assume you can do this if I can. Two years ago I tried this, getting the left hand on the steering wheel at the 11 o'clock position. But failed because my bicep spasticity was stronger than my finger spasticity for grasping. I have to do this in town on stretches of straight road because I have to uncurl my fingers to get them on the wheel. The freeway doesn't work because accelerating down the on ramp at the same time as trying to get the fingers on the wheel doesn't work. My right arm is always available to immediately knock my left arm off the wheel if necessary. This does require the crossover turn signal extender since I never would be able to reach around my left arm to get at the regular turn signal. There is no ability to look over my left shoulder into my blind spot for cars, I'm limited to constantly checking mirrors.  I'm back to 100+% attention to driving again, same as when I started driving.  The tiny corrections needed to keep the car in the lane are great for maybe finally getting some use out of my arm and hand.  I can see in the distant future the ability to drink coffee, change CDs, radio stations and look at passengers when talking to them.

Ten definitions of resilience with respect to the degree of normativity

You will need massive amounts of resilience in order to recover. What is your doctor doing to assist you in that endeavor?
1) Original-ecological Measure of the persistence of systems and of their ability to absorb change and disturbance and still maintain the same relationships between populations or state variables Holling 1973:14

2) Extended-ecological The magnitude of disturbance that can be absorbed before the system changes its structure by changing the variables and processes that control behavior
The capacity of a system to experience shocks while retaining essentially the same function, structure, feedbacks, and therefore identity
Gunderson and Holling 2002:4

Walker et al. 2006:2

2a) Three characteristics capacities i) to absorb disturbances, ii) for self-organization, and iii) for learning and adaptation Walker et al. 2002

2b) Four aspects 1) latitude (width of the domain),
2) resistance (height of the domain),
3) precariousness,
4) cross-scale relations
Folke et al. 2004:573

3) Systemic-heuristic Quantitative property that changes throughout ecosystem dynamics and occurs on each level of an ecosystem’s hierarchy Holling 2001

4) Operational Resilience of what to what?
The ability of the system to maintain its identity in the face of internal change and external shocks and disturbances
Carpenter et al. 2001
Cumming et al. 2005
5) Sociological The ability of groups or communities to cope with external stresses and disturbances as a result of social, political, and environmental change Adger 2000:347

6) Ecological-economic Transition probability between states as a function of the consumption and production activities of decision makers
The ability of the system to withstand either market or environmental shocks without loosing the capacity to allocate resources efficiently
Brock et al. 2002:273

Perrings 2006:418
7) Ecosystem-services-related The underlying capacity of an ecosystem to maintain desired ecosystem services in the face of a fluctuating environment and human use Folke et al. 2002:14

8) Social-ecological system

8a) Social-ecological The capacity of a social-ecological systems to absorb recurrent disturbances (...) so as to retain essential structures, processes and feedbacks Adger et al. 2005:1036

8b) Resilience-approach A perspective or approach to analyze social-ecological systems Folke 2006
9) Metaphoric Flexibility over the long term Pickett et al. 2004:381

10) Sustainability-related Maintenance of natural capital in the long run Ott and Döring 2004:213f

3 Hidden Signs that Someone is a Psychopath

I even managed to miss all three signs.
The coffee was a suprising one.

They’re immune to yawning stimuli

They tend to take a lot of selfies - men

They order black coffee


Physical Activity Benefits Creativity: Squeezing a Ball for Enhancing Creativity - stroke recovery

You're going to have to become creative with your recovery because your doctor has no clue how to get you 100% recovered. Get your mind out of the gutter, this is serious stuff. Your doctor should be able to tell you which hand used is better for creativity. Your affected one? Or your 'good' one?
JongHan Kima*
pages 328-333


Studies in embodied cognition show that physical sensations, such as touch and movement, influence cognitive processes. Two studies were conducted to test whether squeezing a soft versus a hard ball facilitates different types of creativity. Squeezing a malleable ball would increase divergent creativity by catalyzing multiple or alternative ideas, whereas squeezing a hard ball would increase convergent creativity by facilitating only a single correct response. In Study 1, participants squeezed either a hard ball or a soft ball while completing the Torrance Test of Creative Thinking (TTCT), a divergent creativity test. The same procedures were used in Study 2 except that the TTCT was replaced with the Remote Associates Test, a convergent creativity test. Participants who squeezed a soft ball generated more original and diverse ideas (Study 1), whereas participants who squeezed a hard ball were better at coming up with a single correct answer (Study 2).

Paper Raises More Questions About Salt Restriction In Heart Failure

You'll have to have your doctor weigh in on this. I wonder what this means for blood pressure? It seems that salt restriction is based on appeal to authority.

If Health Care Worked Like Amazon - stroke version

Dr. Toni Brayer wrote the original.
I added a few points that stroke should have;
  1. Your doctor has a 3d rotatable map of your brain and its' dead and damaged areas. Each area is labeled with what the external effects or disabilities from the damage is.
  2. Each effect/damaged area has stroke protocols attached with efficacy ratings.
  3. Your medical wearables tell you if you are doing the suggested exercises from the protocols correctly.  No real need for actual therapist contact.
  4. No real need for a doctor either.

Developing drugs to reduce brain impairment after stroke -CAL-101 to block TNF

An easier to understand writeup on TNF blocking. Don't expect anything from this to reach your hospital for at least 50 years.

Developing drugs to reduce brain impairment after stroke

Stroke claims five million lives worldwide each year and is the second biggest killer after ischaemic heart disease. Of those who survive, a significant number (around five million) live with neurological deficits that profoundly affect their quality of life.
Current treatment for ischaemic stroke, which results from a blood clot, aren’t very effective (Only 12%). But research published by my colleagues and I today in the journal Nature Communications shows an emerging drug treatment is effective in mice and could one day reduce the neurological impact in people who’ve suffered an ischaemic stroke.
By 2020, the World Health Organization predicts that worldwide, the number of years lost to disability resulting from stroke will reach 61 million. The economic burden is similarly massive, costing Australia $49.3 billion a year. So finding better treatments is crucial.

Brain inflammation after stroke

Quick treatment is one way to enhance the prospect of recovering from a stroke.
If patients are treated within around three hours of the stroke, the stroke-inducing clots can be broken down relatively efficiently(Only 12% is not very effective) using a substance called tissue plasminogen activator (tPA). This allows the blood to start flowing again, supplying the brain with the oxygen required to keep the tissue alive.

But after the clot is removed and blood starts flowing, the body produces an unwanted neuroimmune response. This occurs because the damaged brain tissue contains elevated levels of molecules known as proinflammatory cytokines, which regulate the body’s response to infection, inflammation and trauma.
These cytokines are able to recruit many other immune cells to the area, leading to further cell death.
Limiting the initial release of these cytokines should therefore help to decrease the excessive local inflammatory response, leading to a decrease in tissue damage and better patient outcomes.

Targeting a critical molecule

A key cytokine involved in this process is tumour necrosis factor-α (TNF-α). In previous work, we showed that the secretion of TNF-α is dependent on a molecule named phosphoinositide 3-kinase delta (PI3Kδ). For our latest study, we hypothesised that PI3Kδ could be similarly involved in stroke.
In collaboration with Garrie Arumugam from the University of Queensland, researchers at Monash University and international colleagues in London and Hamburg, we induced strokes in mice to demonstrate that – as expected – PI3Kδ controlled the release of TNF-α from immune cells of the central nervous system.
This suggested to us that by inhibiting PI3Kδ activity, we would be able to prevent the rise in TNF-α secretion and therefore limit inflammation of the brain and cell death.
Two separate lines of evidence indicated this was the case: mice genetically modified to have inhibited PI3Kδ activity had only limited TNF-α release, and mice that were given the PI3Kδ-inhibiting drug CAL-101 showed similar effects.
Further, blocking PI3Kδ activity (through genetic manipulation or medication) decreased blood clot-induced brain damage and resulted in improved performance on neurological tests.

These results indicate that we successfully identified a pathway critical to post-treatment inflammation of the brain, and that we could limit the damage by blocking PI3Kδ, a key molecule within that pathway.
While the genetic manipulation played a role in identifying the signalling pathway involved, it is the efficacy of CAL-101 that is particularly exciting and relevant to stroke therapy. Not only was the drug effective in improving post-stroke recovery, but its effects could be seen when given up to three hours after the clot was removed and blood started flowing.
Since initial stroke treatment is typically initiated by medically trained staff, CAL-101 (or a related molecule) could potentially be injected alongside tPA to reduce inflammation of the brain and improve patient outcomes.

Taking it to the clinic

The next obvious question is whether CAL-101 or a similar derivative may ultimately be used to improve stroke treatment in humans.
Our study was conducted in mice, and translating findings in animal models to the development of clinical therapies can be very difficult – clinical trials of drugs fail frequently due to safety or efficacy concerns.
In positive news, however, CAL-101 (also known as GS-1101 or idelalisib) has recently undergone phase three clinical trials in the United States for the treatment of certain forms of lymphoma and the results look promising.
CAL-101 is therefore a very promising molecule. Not only does it treat lymphomas, it has the potential to alleviate the complications that arise following initial stroke treatment. We’re now also looking into other medical conditions that could be improved by reducing inflammation of the brain with CAL-101 or a similar compound.

PI3Kδ inhibition reduces TNF secretion and neuroinflammation in a mouse cerebral stroke model

The whole basis of Dr. Tobinicks use of etanercept is to interfere with TNF. Whom will do the followup research on this? This will never be followed up since we have NO stroke leadership we can bring these simple questions to. Every stroke survivor for the next 50 years is going to be screwed because nothing is going to get done until WE take over all the stroke associations.
If Dr. Tobinick cared at all about proving if his ideas are correct he would have followed up this research from March 2014 with clinical research trials. 
Nature Communications
Article number:


Stroke is a major cause of death worldwide and the leading cause of permanent disability. Although reperfusion is currently used as treatment, the restoration of blood flow following ischaemia elicits a profound inflammatory response mediated by proinflammatory cytokines such as tumour necrosis factor (TNF), exacerbating tissue damage and worsening the outcomes for stroke patients. Phosphoinositide 3-kinase delta (PI3Kδ) controls intracellular TNF trafficking in macrophages and therefore represents a prospective target to limit neuroinflammation. Here we show that PI3Kδ inhibition confers protection in ischaemia/reperfusion models of stroke. In vitro, restoration of glucose supply following an episode of glucose deprivation potentiates TNF secretion from primary microglia—an effect that is sensitive to PI3Kδ inhibition. In vivo, transient middle cerebral artery occlusion and reperfusion in kinase-dead PI3Kδ (p110δD910A/D910A) or wild-type mice pre- or post-treated with the PI3Kδ inhibitor CAL-101, leads to reduced TNF levels, decreased leukocyte infiltration, reduced infarct size and improved functional outcome. These data identify PI3Kδ as a potential therapeutic target in ischaemic stroke.

Could big data and wearables help the fight against diseases? Applicable to stroke?

We'll never know because we have NO stroke strategy or stroke leadership in any part of stroke.

Improving Human Activity Recognition and its Application in Early Stroke Diagnosis

Stroke diagnosis is pretty much a failure right now. Would anything here be better?  
Test out these 17 diagnosis possibilities to find out which one is the best?  Or maybe the Qualcomm Xprize for the tricorder?
José R. Villar
  • Corresponding author.
  • Computer Science Department, University of Oviedo, ETSIMO, Oviedo, Asturias 33005, Spain
  • Silvia González
  • Instituto Tecnológico de Castilla y León c/López Bravo 70 Burgos, Burgos 09001, Spain
  • Javier Sedano
  • Instituto Tecnológico de Castilla y León c/López Bravo 70 Burgos, Burgos 09001, Spain
  • Camelia Chira
  • Computer Science Department, Tech. University of Cluj-Napoca, 28 Gh. Baritiu Street, 400027 Cluj-Napoca, Romania
  • Jose M. Trejo-Gabriel-Galan
  • Neurology Department of the Burgos' Hospital, Burgos, Spain
  • Accepted: 4 November 2014
    Published: 16 February 2015
    The development of efficient stroke-detection methods is of significant importance in today's society due to the effects and impact of stroke on health and economy worldwide. This study focuses on Human Activity Recognition (HAR), which is a key component in developing an early stroke-diagnosis tool. An overview of the proposed global approach able to discriminate normal resting from stroke-related paralysis is detailed. The main contributions include an extension of the Genetic Fuzzy Finite State Machine (GFFSM) method and a new hybrid feature selection (FS) algorithm involving Principal Component Analysis (PCA) and a voting scheme putting the cross-validation results together. Experimental results show that the proposed approach is a well-performing HAR tool that can be successfully embedded in devices.

    Neuroplasticity: Achieve the Best Outcomes with Neurological Patients

    This PT doesn't understand the neuronal cascade of death at all.
    One sentence from there.
    Still, there is also a need for caution, since intense early activity may actually increase lesion size, with exaggerated functional loss especially in the first 7 days.
    Wrong, wrong, wrong. This has nothing to do with activity, The neuronal cascade of death is running its course.

    Low Blood Flow in Back of Brain Increases Risk of Recurrent Stroke

    Info if this applies to you. Doctor question.
    Patients who have had a stroke in the back of the brain are at greater risk of having another within 2 years if blood flow to the region is diminished, according to a study published in JAMA Neurology.
    These patients are the most likely to benefit from risky intervention to unblock arteries, and they can be identified using a new magnetic resonance imaging (MRI)-based technology developed at the University of Illinois at Chicago, Chicago, Illinois.
    “Having a blockage present in a blood vessel doesn’t always correlate to low blood flow,” said principal investigator Sepideh Amin-Hanjani, MD, University of Illinois at Chicago College of Medicine. “There can be a blockage and flow can be normal, if other nearby blood vessels are able to compensate.”
    The researchers wanted to try to identify which patients who had experienced a stroke were at highest risk for further strokes and so might benefit from angioplasty despite the risks of the procedure.
    They followed 72 adult patients who had a stroke or a transient ischemic attack (TIA) in the back of the brain and who also had at least 50% blockage of the arteries in that part of the brain. The patients were followed for an average of 22 months at 5 academic medical centres as they continued receiving standard care for their condition from their neurologists.
    Patients were evaluated for reduced blood flow in the back of the brain using Non-Invasive Optimal Vessel Analysis (NOVA), a software program that can quantify the volume, velocity, and direction of blood flowing through any major vessel in the brain using standard MRI equipment.
    One-fourth of the patients were found to have diminished blood flow in the back of the brain, which turned out to be a significant predictor of subsequent stroke. These patients had 12- and 24-month stroke-free survival rates of 78% and 70%, respectively, compared to 96 percent and 87 percent for patients with normal blood flow.
    “At 1 year, the risk for patients with low blood flow was about 5 times as high as risk for patients without low flow in the back of the brain,” said Dr. Hanjani.
    For these patients, the benefits of angioplasty probably outweigh the risks.
    “About three-quarters of patients didn't have low blood flow in the vertebrobasilar region and these patients would not benefit from treatments aimed at opening the vessels, such as angioplasty,” said Dr. Hanjani. “In fact, the procedure would put these patients at unnecessary risk.”
    The ultimate goal is to find what treatments might be most effective for each patient, he added.
    The researchers hope that the ease of identifying the high-risk group using NOVA will enable further study of the condition and the evaluation of new therapies to further reduce the risk of recurrent stroke.
    SOURCE: University of Illinois at Chicago

    Brain Death Determinations Vary Across Hospitals

    I wonder what the explanation is used on death certificates for people dying from stroke effects. People do not die from the stroke, they die from brain damage. Until this reporting is changed we never will be able to determine the reason for dying. Stoke is way too simplistic and uninformative. We used to have the category of dying from old age, that was eliminated because it told us nothing useful.

    Wednesday, December 30, 2015

    Leaving Facebook group Young Stroke Survivors

    Don't worry James Cooper, after this response is published I will be removing myself from this group  before I get banned. I assume that this will also be deleted so I will be putting it on my blog where I only have had 1.7  million views. I see no reason to belong to a group where legal research and lobbying possibilities are not discussed. Going down the route of medical marijuana is only useful if that is the only way to take the next step of full legalization. The state statutes I've looked at don't allow use for stroke. With 10 million stroke survivors a year we can easily influence public policy but only if we can discuss the options. If you want to be a part of the problem along with all the stroke associations, neurologists and PMR doctors that is your choice. The status quo in stroke is appalling and the only way to change that is to take matters into our own hands. My post on The Way Forward details my ideas on what needs to be done.

    Educate yourself.  I've written 78 posts on marijuana 
    20 on medical marijuana
    2 on THC
    18 on cannabinoid
    6 on cannabis
    with this one covering covering it most concisely if you want to be enlightened; My 13 reasons for marijuana use post-stroke.  Or maybe this; Treating brain diseases with marijuana  
    You can easily dismiss me because I have no medical training, which actually is a plus since our stroke medical professionals have been failing survivors for decades. Good luck on recovery for your children and grandchildren from stroke if WE don't take charge of everything in stroke. I plan on paying it forward, do you?


    This might work for those that don't need ankle support for foot rolling.  But remember you can't tell your therapist about solution possibilities because neither you nor I are medically trained.
    A comment came in via email from a representative;
    'With regard to support for weak ankles and rolling, we find that the adjustable straps help to keep the foot straight when walking.  For example, if your foot pulls to one side, you can tighten the strap on the other side.  This will help to minimize some rolling.  The heavy duty, custom spring allows for both dorsi and plantar flexing (keeping the leg muscles active).  And the cuff has a 1/4” neoprene liner for all day comfort; it can also adjusted for any swelling during the day.'
    The KX2 Flexible Foot Liftpictured above with the eyelet hook attachment
    The KX2 Flexible Foot Liftpictured above with the toe strap attachment.

    Maybe you want to remind your therapist about all these other possibilities;
    Bioness L300
    300PV FES

    or these
    1. Soft brace -
    2.. Musmate a strapping and bungee sytem -
    3. x-strap a bungee sytem from the ankle -
    4. Malleoloc Ankle Brace -
    5. surgery
    6. AFO hinged or fixed
    or do nothing which is what your insurance will pay for.
    I also have 38 posts on AFOs for those with extreme need for complete boringness.

    Ontario Stroke Evaluation Report 2011: Improving System Efficiency by Implementing Stroke Best Practices

    And not a single word in this report states that stroke care is a complete failure because only 10% get to almost full recovery. Just 'Happy talk'. If there are no problems found making things better will never occur. You don't compare yourself to the status quo, you compare yourself to the ideal recovery.  Best practices that only get 10% to full recovery is a complete failure. Own up to your failures. No best practice for anything to do with the neuronal cascade of death. I guess neurons dying in the first week is nothing to be concerned about.

    Tuesday, December 29, 2015

    New Alzheimer’s treatment fully restores memory function

    Lucky if you are a mouse with Alzheimers.
    Australian researchers have come up with a non-invasive ultrasound technology that clears the brain of neurotoxic amyloid plaques - structures that are responsible for memory loss and a decline in cognitive function in Alzheimer’s patients.
    If a person has Alzheimer’s disease, it’s usually the result of a build-up of two types of lesions - amyloid plaques, and neurofibrillary tangles. Amyloid plaques sit between the neurons and end up as dense clusters of beta-amyloid molecules, a sticky type of protein that clumps together and forms plaques.
    Neurofibrillary tangles are found inside the neurons of the brain, and they’re caused by defective tau proteins that clump up into a thick, insoluble mass. This causes tiny filaments called microtubules to get all twisted, which disrupts the transportation of essential materials such as nutrients and organelles along them, just like when you twist up the vacuum cleaner tube.
    As we don’t have any kind of vaccine or preventative measure for Alzheimer’s - a disease that affects 343,000 people in Australia, and 50 million worldwide - it’s been a race to figure out how best to treat it, starting with how to clear the build-up of defective beta-amyloid and tau proteins from a patient’s brain. Now a team from the Queensland Brain Institute (QBI) at the University of Queensland have come up with a pretty promising solution for removing the former.
    Publishing in Science Translational Medicine, the team describes the technique as using a particular type of ultrasound called a focused therapeutic ultrasound, which non-invasively beams sound waves into the brain tissue. By oscillating super-fast, these sound waves are able to gently open up the blood-brain barrier, which is a layer that protects the brain against bacteria, and stimulate the brain’s microglial cells to activate. Microglila cells are basically waste-removal cells, so they’re able to clear out the toxic beta-amyloid clumps that are responsible for the worst symptoms of Alzheimer’s.
    The team reports fully restoring the memory function of 75 percent of the mice they tested it on, with zero damage to the surrounding brain tissue. They found that the treated mice displayed improved performance in three memory tasks - a maze, a test to get them to recognise new objects, and one to get them to remember the places they should avoid.
    "We’re extremely excited by this innovation of treating Alzheimer’s without using drug therapeutics," one of the team, Jürgen Götz, said in a press release. "The word ‘breakthrough’ is often misused, but in this case I think this really does fundamentally change our understanding of how to treat this disease, and I foresee a great future for this approach."
    The team says they’re planning on starting trials with higher animal models, such as sheep, and hope to get their human trials underway in 2017. 
    You can hear an ABC radio interview with the team here.

    Increased return of spontaneous circulation at the expense of neurologic outcomes: Is prehospital epinephrine for out-of-hospital cardiac arrest really worth it?

    So you need to know this side effect of ambulance treatment of cardiac arrest. You may not want poor neurologic outcome. But don't listen to me, I'm not medically trained, I just read a lot. Of course you'll be unconscious in seconds so you'll have no say in the matter.

    Heart Attack vs. Sudden Cardiac Arrest: Understanding the Difference

    Journal of Critical Care 30 (6), 1376-81 (Dec 2015)

    INTRODUCTION Current guidelines for the management of out-of-hospital cardiac arrest (OHCA) recommend the use of prehospital epinephrine by initial responders. This recommendation was initially based on data from animal models of cardiac arrest and minimal human data, but since its inception, more human data regarding prehospital epinephrine in this setting are now available. Although out-of-hospital return of spontaneous circulation (ROSC) may be higher with the use of epinephrine, worse neurologic outcomes may be associated with its use.
    METHODS A systematic review of the literature was conducted by search of databases including PubMed, Embase, and OVID to identify studies comparing patients with OHCA who had received epinephrine before arrival to the hospital with those who had not. Studies were assessed for quality and bias, and data were abstracted from studies deemed appropriate for inclusion. A meta-analysis was conducted using a Mantel-Haenszel model for dichotomous outcomes. Outcomes studied were prehospital ROSC, survival at 1 month, survival to discharge, and positive neurologic outcome.
    RESULTS A total of 14 studies with 655853 patients were included for the meta-analysis. The use of epinephrine for OHCA before arrival to the hospital was associated with a significant increase in ROSC (odds ratio, 2.86; P<.001) and a significant increase in the risk of poor neurologic outcome at the time of discharge (odds ratio 0.51, P = .008). There was no significant difference in survival at 1 month or survival to discharge.
    CONCLUSION Use of epinephrine before arrival to the hospital for OHCA does not increase survival to discharge but does make it more likely for those who are discharged to have poor neurologic outcome. There is a need for additional randomized controlled trials.

    NeuroRecovery Training Institute Announces Stroke Specialty Certification

    Before your therapist goes to this, these questions should be asked of the instructors. 'What percentage of your patients get to 100% recovery?'  'What guarantees of recovery will be able to be provided to survivors from use of this course?'
    This ought to be really interesting since the only evidence based therapy is CIMT. Hell, therapists don't even have a common protocol to get patients walking.
    The NeuroRecovery Training Institute (NeuroRTI) is proud to announce they will be offering a Stroke Specialty Certification beginning March 2016.
    This 11-15 month program of post-professional clinical and didactic education is designed to translate evidence into practice, providing both physical and occupational therapists with the tools to deliver best practice management to the post-stroke population. The evidence-based curriculum will guide participants through the full spectrum of stroke rehabilitation, from neuroanatomy and pathology to examination and treatment, with the ultimate goal of facilitating recovery of function and improved reported quality of life. This program will be led by Jill Seale, PT, PhD, NCS, and Rachelle Studer-Byrnes, PT, DPT, NCS.
    “We are thrilled to be launching the Stroke Specialty Certification and are eager to introduce the course material to students come March,” said Seale.
    “We look forward to empowering students who are passionate about working with stroke survivors and providing them with the tools to promote recovery post-stroke and improve their patients’ outcomes and quality of life,” added Studer-Byrnes.
    Cohorts will launch in March, July, and September of 2016. For admission requirements, curricula details, and total hours and credits, please visit
    About The NeuroRecovery Training Institute
    The NeuroRecovery Training Institute (NeuroRTI) is on a mission to create and promote a culture of evidence-based practice (EBP) within neurological clinical practice. Through transformational education efforts, with an emphasis on recovery NeuroRTI has created a full continuum of neurologic training programs including a large nationally-scaled physical therapy Neuro Residency, Postprofessional DPT, Certification, and online Continuing Education (CE) course work for the neurologic interdisciplinary team that includes various topics in the treatment of spinal cord dysfunction, acquired brain injury, and other neurologic disorders. A course on the Pediatric Neuromuscular Recovery Scale, a recovery based outcomes tool will launch in early 2016.

    Drink A Cup Of Coffee Before Working Out And It Might Boost Endurance, Enhance Performance

    How many decades before your OTs and PTs give you a cup of coffee before a therapy session? I'm betting never since we have no one to research such a simple question.
    Coffee is ingrained in many people’s early morning routines because they rely on its mildly stimulating effect to get them going for the day. In addition to keeping people from crawling back to bed and eluding their responsibilities in the morning, the world’s favorite hot beverage can also help people power through long grueling workouts, according to new research published in the International Journal of Sport Nutrition and Exercise Metabolism.
    Although endurance athletes commonly ingest caffeine in the form of powder or tablets as a means to enhance training intensity and competitive performance, conflicting evidence exists regarding the efficacy of coffee — a popular source of caffeine — in improving athletic performance. Unsure of coffee’s effect on performance, researchers conducted a meta-analysis review to evaluate how pre-exercise coffee impacts endurance performance.
    "There's a perception that coffee won't give you the same benefits as pure caffeine," study lead author Simon Higgins said in a statement. "New research could mean that athletes could have a cup of coffee versus taking a pill."
    Caffeine, the most popular psychoactive substance among people of all age groups and cultural backgrounds, is typically used to boost the central nervous system for cognitive or physical endeavors. The stimulant is produced by a variety of beans, leaves, and fruits, but is most commonly consumed in the form of coffee, according to the National Council on Strength and Fitness (NCSF).
    For the study, Higgins and his colleagues reviewed nine randomized control trials that specifically used coffee to improve endurance. During the trials, study participants either cycled or ran after drinking coffee. They then exercised vigorously, and the results were measured.
    Researchers from five studies found significant improvements in endurance performance. They found between 3 and 7 milligrams per kilogram of body weight of caffeine from coffee increased endurance performance by an average of 24 percent. The amount of caffeine in a cup of coffee can vary from 75 milligrams to more than 150, depending on the variety and how it's roasted and brewed. Americans consume about 27 ounces of coffee each day, Medical News Today reported.
    "This is helpful for athletes because coffee is a naturally occurring compound," Higgins said. "There's the potential that getting your caffeine by drinking coffee has similar endurance benefits as taking caffeine pills."
    Previous studies have linked coffee to many health benefits, including a reduced risk of dying from cardiovascular disease, an extended lifespan, and a lower risk of developing type 2 diabetes.
    Higgins said the endurance effects of coffee as a source of caffeine could be just as advantageous as taking caffeine in the form of powder or tablets.
    "While there is a lack of high-quality research on coffee as a source of caffeine, there is an abundance of research on pure caffeine," he said. "It's surprising how little we know about caffeine from coffee when its endurance effects could be just as beneficial as pure caffeine."
    Nevertheless, before any recommendations can be given to athletes, more research will be needed to determine how different the effects of caffeine from coffee are against those from pure caffeine — especially since the amount of caffeine in a cup of coffee can vary.

    How Does Marijuana Affect the Brain and Behavior? Here's What Recent Studies Say

    My God, anything to put a negative spin on marijuana. We already know that young brains aren't fully developed until 26-28, so unless we know the age of the participants this may not be a valid conclusion. We'll never know because we have NO stroke strategy or stroke leadership in any part of stroke. But Reefer Madness strikes again.
    The sky is falling article here:

    How Does Marijuana Affect the Brain and Behavior? Here's What Recent Studies Say

    Actual research article here: It references young adults. Can't tell who sponsored the research.

    Effects of marijuana use on impulsivity and hostility in daily life

    Monday, December 28, 2015

    D-4F Decreases White Matter Damage After Stroke in Mice

    We'll never know if this would help in humans because we have NO stroke strategy or stroke leadership in any part of stroke.

    1. Jieli Chen, MD
    + Author Affiliations
    1. From the Department of Neurology, Henry Ford Hospital, Detroit, MI (X.C., M.C., A.Z., C.C., T.Y., R.N., J.C.); and Department of Physics, Oakland University, Rochester, MI (M.C.).
    1. Correspondence to Jieli Chen, MD, Neurology Research, E&R Bldg, Room No 3091, Henry Ford Hospital, 2799 W Grand Blvd, Detroit, MI 48202. E-mail


    Background and Purpose—Stroke-induced neuroinflammation and white matter damage are associated with neurological deficits. Whether D-4F, an apolipoprotein A-I mimetic peptide, treatment of stroke decreases neuroinflammation and white matter damage and improves functional outcome has not been investigated.
    Methods—Adult male C57BL/6 mice were subjected to permanent middle cerebral artery occlusion (MCAo) and were orally administered saline as a vehicle control and different doses of D-4F (2, 4, 8, 16, or 32 mg/kg) starting at 2 h after MCAo and daily until euthanized at 7 days after MCAo. D-4F treatment did not alter the blood levels of high-density lipoprotein, total cholesterol, triglyceride, blood–brain barrier leakage, and infarction volume compared with control group.
    Results—D-4F (16 mg/kg) treatment of stroke significantly improved functional outcome, increased the white matter density and the number of oligodendrocyte progenitor cells in the ischemic boundary zone of the ipsilateral striatum, and increased myelin basic protein, insulin-like growth factor-1 (IGF1), but decreased inflammatory factor Toll-like receptor-4 and tumor necrosis factor-α expression in the ischemic brain 7 days after MCAo (P<0.05, n=11/group). The neurite/axonal outgrowth in primary cultured neurons was significantly increased when treated with D-4F (100 ng/mL) and IGF1 (100 ng/mL) compared with the nontreatment control. Inhibition of IGF1 significantly attenuated D-4F or IGF1 treatment–induced axonal outgrowth. D-4F-treatment did not increase oligodendrocyte–progenitor cell proliferation but decreased oligodendrocyte–progenitor cell death.
    Conclusions—D-4F treatment initiated 2 h after MCAo decreases neuroinflammation and white matter damage and improves functional outcome after stroke. D-4F-induced increase in IGF1 may contribute to D-4F–induced neurite/axonal outgrowth after stroke.

    Stroke Location Is an Independent Predictor of Cognitive Outcome

    DUH! Do you have to be smarter than a fifth grader to know that? My stroke blew out my motor and premotor cortex, so I would expect my cognition not to be affected.

    1. Thomas Tourdias, MD, PhD
    + Author Affiliations
    1. From the Université de Bordeaux, Bordeaux, France (F.M., C.R.G., V.D., I.S., T.T.); Neuroimagerie diagnostique et thérapeutique (F.M., A.B., V.D., T.T.), Unité neurovasculaire (S.S., S.D., M.P., P.R., I.S.), and Pôle de santé publique, Unité de Soutien Méthodologique à la Recherche Clinique et Epidémiologique (J.A., P.P.), CHU de Bordeaux, Bordeaux, France; INSERM, U862, Neurocentre Magendie, Bordeaux, France (F.M., V.D., T.T.); Center for Neurological Imaging, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA (C.R.G.); and INCIA, Bordeaux, France (I.S.).
    1. Correspondence to Thomas Tourdias, MD, PhD, Neuroradiology, CHU de Bordeaux, Bordeaux University Hospital, Place Amélie Raba-Léon, Bordeaux F-33076, France. E-mail


    Background and Purpose—On top of functional outcome, accurate prediction of cognitive outcome for stroke patients is an unmet need with major implications for clinical management. We investigated whether stroke location may contribute independent prognostic value to multifactorial predictive models of functional and cognitive outcomes.
    Methods—Four hundred twenty-eight consecutive patients with ischemic stroke were prospectively assessed with magnetic resonance imaging at 24 to 72 hours and at 3 months for functional outcome using the modified Rankin Scale and cognitive outcome using the Montreal Cognitive Assessment (MoCA). Statistical maps of functional and cognitive eloquent regions were derived from the first 215 patients (development sample) using voxel-based lesion-symptom mapping. We used multivariate logistic regression models to study the influence of stroke location (number of eloquent voxels from voxel-based lesion-symptom mapping maps), age, initial National Institutes of Health Stroke Scale and stroke volume on modified Rankin Scale and MoCA. The second part of our cohort was used as an independent replication sample.
    Results—In univariate analyses, stroke location, age, initial National Institutes of Health Stroke Scale, and stroke volume were all predictive of poor modified Rankin Scale and MoCA. In multivariable analyses, stroke location remained the strongest independent predictor of MoCA and significantly improved the prediction compared with using only age, initial National Institutes of Health Stroke Scale, and stroke volume (area under the curve increased from 0.697–0.771; difference=0.073; 95% confidence interval, 0.008–0.155). In contrast, stroke location did not persist as independent predictor of modified Rankin Scale that was mainly driven by initial National Institutes of Health Stroke Scale (area under the curve going from 0.840 to 0.835). Similar results were obtained in the replication sample.
    Conclusions—Stroke location is an independent predictor of cognitive outcome (MoCA) at 3 months post stroke.

    Saliva Test can Reveal Antibodies That Predict Your Risk Of Mortality

    Is your doctor going to be testing this and helping to adjust this to make sure you live longer?
    Most people would like a forewarning if they’re at a higher risk of death than other people. Some clues are obvious: If you’re ingesting healthy foods, for example, you live longer. But sometimes we can find signals in unexpected places; like clues to your mortality may be in your spit. Seriously. Researchers have discovered that a lower level of antibodies in saliva are associated with an elevated risk of dying, and could function as an early indicator of said risk.
    The research, published by a team from the University of Birmingham, explored the association between an antibody commonly found in saliva (secretory immunoglobin A, or IgA), and mortality rates in the general population. They looked at 639 adults aged 63 or older at the time of saliva sampling in 1995, and measured their IgA secretion rates. The participants were then tracked for mortality over the following 19 years, with any associations being measured for gender, occupational group, smoking, and medication usage.
    There ended up being a negative association between IgA secretion rate and all-cause mortality. A deeper analysis of the data showed that the all-cause association was possibly due to an underlying association with cancer mortality particularly with non-lung cancers.
    Immunoglobulins, also called antibodies, are proteins the white blood cells secrete. They are essential for combating infectious diseases.
    “There are a number of factors that can affect how well we produce antibodies and maintain their levels,” explained Dr. Anna Phillips, from the University of Birmingham, in a press release. “There are some we have no control over, such as age, heritability or illness, but our general state of health can also affect their levels: stress, diet, exercise, alcohol, and smoking can all influence those levels.”
    Phillips says that it remains to be seen exactly how saliva samples could be used in check-ups, since researchers need to better understand the line at which the secretion rate should be considered a cause of concern. “We could certainly say that, if found to be extremely low, it would be a useful early indicator of risk,” she said.
    The team believes its next step should be a larger, longitudinal study to follow up and investigate the link between their findings and infectious diseases. They would also like to examine the development progression of a disease such as cancer to provide a greater understanding of the mechanisms behind the association detailed in the study.
    Study: Phillips A, Carrol D, Drayson M, Der G. Salivary Immunoglobin A Secretion Rate is Negatively Associated with Cancer Mortality: the West of Scotland Twenty-07 Study. PLOS One. 2015.

    “Most of our troubles are due to our passionate desire for and attachment to things that we misapprehend as enduring entities.” ~Dalai Lama

    This is probably one of the reasons why I stayed in a disastrous marriage for so long. Another great Tiny Buddha post.
    Letting Go of Attachment: From A to Zen

    Matching challenge doubles your gift's impact - National Stroke Association

    And none of this will do one bit of good toward solving all of the problems in stroke. This is just to make you feel good and relieve you of some money.  More 'Happy talk'. Matt Lopez, you need to explain why your organization is not doing one concrete thing for future survivors. Like maybe lessening their disability from the stroke. Learn what cause and effect is and attack the causes of stroke disability. Do you even know about the neuronal cascade of death?
    View this message on our website.
    Double your gift to National Stroke Association

    Dear dean,

    Be part of our Matching Gift Challenge

    Double your gift to National Stroke Association
    Give today
    When you make a tax-deductible donation to National Stroke Association by Dec. 31, you help us take advantage of a matching gift challenge generously supported by REACH Health.
    • A gift of $50 becomes $100 which helps to get the word out about how knowing the symptoms of stroke and how what you do in the first minutes after a stroke can save lives and preserve brain function.
    • A contribution of $80 becomes $160 to help pair a Stroke Recovery Navigator with a stroke survivor during the critical six months following a stroke when they are struggling to find their bearings and move forward with life.
    • A donation of $150 becomes $300 to provide resources to encourage, support, and train family members in the proper care of stroke survivors. 
    Today, more than ever, you can make a profound difference in the life of someone you love by giving a tax-deductible gift to National Stroke Association.
    Thank you for your support. It means so much!
    Warmest wishes,
    signed by Matt Lopez, CEO
    Matt Lopez
    CEO, Stroke Survivor