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:http://oc1dean.blogspot.com/2010/11/my-background-story_8.html

Thursday, June 30, 2016

The Illicit Drug That Removes Toxic Alzheimer’s Proteins - Marijuana

This will never legally occur with our stupid federal legislators in charge. Unless YOU get your Mom and grandma to ream them out for not allowing legalization of marijuana.
http://www.spring.org.uk/2016/06/illicit-drug-fights-alhzeimers.php?

4 Things You Need to Know When Pursuing An Ambitious Dream

My dream is to completely change stroke rehab, such that it becomes a minor illness.  It is grandiose and delusional since I have no medical experience and don't even have a clue on how to set up a foundation to accomplish that. I have purchased the URL of strokeresearchinstitute.com so I'm not completely at step zero.
http://tinybuddha.com/blog/4-things-need-know-pursuing-ambitious-dream/

1. There’s no shame in being green.

2. Setbacks are part of the process.

3. It helps to hold yourself accountable.

4. An experience can be worth so much more than it costs.

Full Research Title: "Recognizing left from right arms by individuals with stroke" - stroke laterality study

Participate if you can. Of course you should have already heard about this from your doctor, if any good at all.
http://research.noigroup.com/?_p=stls

1. Introduction

You are invited to participate in this research project which is investigating changes in people (with and without stroke) with upper limb pain. We know from previous research that some people with longstanding hand or arm pain have difficulty recognizing the laterality (left from right) of a picture of their affected hand (perception difficulties).
This research project requires participation from people who have had a stroke, as well as those that haven't, in order that we can make comparisons between these populations.

2. What is the purpose of this research project?

The purpose of this study is to investigate if people with stroke experience difficulty with recognizing the laterality of their affected arm and hand, and if there is a further relationship in those with upper limb pain. This could lead us to better understand upper limb pain in stroke and in turn help us to develop more effective treatment strategies.
To do this we will investigate the accuracy and response time for a left/right judgement task of the shoulder and hand in people who may or may not have had a stroke, and compare the results to those with upper limb pain.
You will need to be aged 18 or over, and have sufficient vision for both reading and looking at images on a computer screen in order to complete this study.

3. Who is conducting this study?

The study is being conducted by Brendon Haslam, a physiotherapist, and will form part of his requirements for the degree of Doctor of Philosophy at the University of Melbourne.
This study is under the supervision of:
  • Professor Leeanne Carey, Florey Institute of Neuroscience and Mental Health at the University of Melbourne, and School of Allied Health at LaTrobe University.
  • Dr David Butler, Neuro Orthopaedic Institute*, Adelaide.
Mr Halton Stewart, from the Neuro Orthopaedic Institute, has been responsible for software research and development.
We have come together to conduct a research project about upper limb pain in stroke. Software development has occurred with the generous support of the Neuro Orthopaedic Institute.
* The Neuro Orthopaedic Institute (NOI) (www.noigroup.com) is an Australian registered company with headquarters in Adelaide. NOI has organised conferences, seminars and university programs in the field of pain and rehabilitation, worldwide for over 25 years. NOI actively supports research in this field. Outcomes of this research may lead to further utilization of their Recognise product as part of future treatment strategies.

4. How much time will the study take?

Participation in this study, involving completion of the online questionnaire and interactive tasks will take approximately 30 minutes. It is possible to take rest breaks between sections which may result in longer times.

5. Procedures

If you agree to participate, you will be asked to complete some simple online questionnaires that involve answering some short questions, followed by looking at simple images on a computer screen and choosing whether these are left or right images. You will be able to complete this from a computer of your choice with internet access.
This study is carried out online and you will be guided through a five step process, involving:
  • Providing consent to participate and information gained to be utilized in research, in addition to consenting to the terms and conditions of the NOI website, available at www.noigroup.com/en/Terms
  • Completion of some questionnaires about yourself, including some questions about your arm (upper limb).
  • Completion of a series of choice reaction tasks, where you will be asked to respond to a series of images by indicating whether it is a left or right image.

6. Possible benefits

While this research will increase knowledge of upper limb pain conditions in stroke and may improve treatment of this condition in the future, we cannot and do not guarantee or promise that you will receive any benefits from the study.

7. Possible risks

Participation in this study should not cause you any discomfort and to our knowledge there are no risks, as supported by previous similar studies.

8. Do I have to take part in this research project?

No. Your participation in this study is entirely voluntary. You are not under any obligation to consent and if you do consent you can withdraw at any time without affecting your relationship with The University of Melbourne, the Neuro Orthopaedic Institute, LaTrobe University or researchers. If you are currently undergoing treatment for upper limb pain, refusal to participate will not influence your management in any way. Whatever your decision, it will not affect your treatment or your relationship with researchers or therapy staff. You can withdraw from the study at any stage by just clicking the exit program link at the bottom of any of the web pages. However, once the study survey is completed, as it is anonymous, your data cannot be withdrawn.

9. How will I be informed of the final results of this research project?

At the completion of the study a report will be prepared that will contain group results. You may access this report via the www.noigroup.com website, and members of the Neuro Orthopaedic Institute database will be informed by mail out/newsletter when this occurs. This report may also be submitted for publication.


10. What will happen to the information about me?

All aspects of the project, including results will be strictly confidential and only researchers involved with the study will have access to your information. Your identity will remain anonymous in data storage systems and in any presentation or publications produced. A report of the study may be submitted for publication, but individual participants will not be identifiable in such a report. Data collected may be accessed for possible future related studies.

11. Can I access research information about me?

As all data collected is anonymous, information about individual participants will not be available, only the collated group data which will be presented in the report as detailed above.

12. Can I ask other people I know to participate?

Yes, the success of this research project relies on large numbers of participants who may or may not have had a stroke. As all information is anonymous, we request that you inform anyone who you think may be interested in participating in this project.

13. Is this research project approved?

This research project has been approved by the Human Research Ethics Committee of The University of Melbourne, in addition to the LaTrobe University Human Ethics Committee.

13. Who can I contact for further information?

If you would like to know more about this research or have any questions regarding this study please feel free to contact the following researchers:
  • Mr Brendon Haslam haslamb@student.unimelb.edu.au
  • Professor Leeanne Carey Leeanne.Carey@florey.edu.au
  • Dr David Butler david@noigroup.com

14. What if I have a complaint or any concerns?

Any person with concerns or complaints about the conduct of this research project and wishes to speak to someone independent of the study investigators, can contact the Executive Officer, Human Research Ethics, The University of Melbourne, Phone:+61 3 8344 2073; Fax +61 3 9347 6739.
You will need to tell the Executive Officer the name of one of the researchers given in the introductory information section above.
*Please save or print a copy of this information sheet for your records

5 Hidden Health Benefits of Alcohol

I'm sure your doctor will never tell you about any benefits of alcohol. Don't start just because you read it here.
Mine are here:

Alcohol for these 12 reasons.  

http://www.livestrong.com/article/557658-5-hidden-health-benefits-of-alcohol/?utm_source=newsletter&

Protect Your Ticker

Beat Belly Bulge

Reduce Risk of Diabetes

Boost Brainpower

Say Goodbye to Gallstones

Details at link.

Lower Levels of Coenzyme Q10 in Blood Associated With Multiple System Atrophy

Do we have any idea what the levels of various markers are supposed to be in survivors compared to normals? An extremely simple question to answer but it won't be because we have fucking failures for stroke associations.
http://dgnews.docguide.com/lower-levels-coenzyme-q10-blood-associated-multiple-system-atrophy?
The neurodegenerative disease known as multiple system atrophy (MSA) affects both movement and involuntary bodily functions. Questions have been raised about the potential role of coenzyme Q10 (CoQ10) insufficiency in the development of MSA. Little is known about blood levels of CoQ10 in patients carrying either COQ2 mutations or no mutations.
Shoji Tsuji, MD, PhD, the University of Tokyo, Tokyo, Japan, and coauthors explored whether there are associations of levels of CoQ10 in the blood and MSA, in a new article published online by JAMA Neurology.
The study included 44 Japanese patients with MSA (average age almost 64) and, for comparison, 39 Japanese control patients (average age about 60).
The authors report their data showed decreased levels of blood CoQ10 in patients was associated with MSA regardless of the COQ2 genotype. The authors suggest this may support the idea that CoQ10 supplementation may be beneficial for patients with MSA. However, they acknowledge study limitations and caution that more studies are needed.
“Prospective cohort studies are warranted to determine the longitudinal effects of plasma levels of CoQ10 on the development of MSA. Furthermore, future clinical trials of supplementation with CoQ10 in patients with MSA are required to confirm our hypothesis,” the article concludes.
SOURCE: JAMA Neurology

Study Shows Sustained IncobotulinumtoxinA Efficacy in Upper-Limb Post-Stroke Spasticity Over 48 Weeks

No clue of what the difference is between this and regular botox injections. Ask your doctor.
It wouldn't have done me any good to ask my doctor about any botox injections because he did nothing, my OT set up the injections.
http://dgnews.docguide.com/study-shows-sustained-incobotulinumtoxina-efficacy-upper-limb-post-stroke-spasticity-over-48-weeks?
For patients with upper-limb post-stroke spasticity, repeated incobotulinumtoxinA injections demonstrated sustained efficacy in reducing muscle tone and spasticity-associated disability, researchers reported here on June 21 at the 20th International Congress of Parkinson’s Disease and Movement Disorders (MDS).
Petr Kaňovský, MD, Faculty of Medicine and Dentistry, Palaký University Olomouc, and University Hospital, Olomouc, Czech Republic, and colleagues have previously shown the 12-week efficacy and safety of incobotulinumtoxinA 400 U versus placebo in patients suffering from upper limb spasticity.
The current study was a 36-week open-label extension period of the main trial.
In the main study, patients were randomised to placebo (n = 107) or incobotulinumtoxinA 400 U (n = 210). Of these, 296 (placebo, 99; incobotulinumtoxinA, 97) continued into this extension study, for three further injections of incobotulinumtoxinA 400 U at 12- to 20-week intervals.
This extension period was completed by 248 patients (82.9%), with outcome measures determined at 4 weeks after each injection.
Outcomes included Ashworth Scale response (≥1-point improvement from each injection to 4 weeks post-injection) and Disability Assessment Scale (DAS) response (≥1-point improvement in a patient-selected principal target domain [hygiene, dressing, limb position or pain] from study baseline to 4 weeks post-injection), adverse events (AEs), and antibody testing.
AS responder rates after each incobotulinumtoxinA treatment were 52.3% to 61.8% for wrist flexors, 49.1% to 60.0% for elbow flexors, 54.5% to 64.5% for finger flexors, 33.9% to 41.2% for thumb flexors, and 37.4% to 44.2% for forearm pronators.
Post-injection DAS responder rates for the principal target domain were 46.2% in the main study, and 52.2%, 62.1, and 59.4% in the extension study injection cycles.
During the main trial, treatment-related AEs were reported in 3.8% and 1.9% of patients receiving incobotulinumtoxinA and placebo, respectively. During the entire 36-week extension study, treatment-related AE incidence was 3.0%. No serious treatment-related AEs and no clinical non-responsiveness due to antibodies occurred in the main trial or in the extension trial.
“These results are impressive because we have a stable response to each injection in this extension period, so incobotulinumtoxinA is effective over the longer period of time, with no serious adverse events at all.”
Funding for this study was provided by Merz Pharmaceuticals GmbH, Germany.
[Presentation title: A Phase 3, Placebo-Controlled Study With an Open-Label Extension: Sustained IncobotulinumtoxinA Efficacy in Upper-Limb Post-Stroke Spasticity Over 48 Weeks. Abstract 956]

Depression, Type 2 Diabetes, and Poststroke Cognitive Impairment

Well, if we had a great stroke association we would know exactly how common dementia is after stroke and how to prevent it. Because we don't you'll just have to flail on your own.
1. A documented 33% dementia chance post-stroke from an Australian study?   May 2012.
2. Then this study came out and seems to have a range from 17-66%. December 2013.
3. A 20% chance in this research.   July 2013.

If you have anything close to a decent doctor a protocol will already be in place to prevent this from occurring. 

http://nnr.sagepub.com/content/early/2016/06/29/1545968316656054.abstract
  1. Walter Swardfager, PhD1,2,3
  2. Bradley J. MacIntosh, PhD1,2
  1. 1Sunnybrook Research Institute, Toronto, Ontario, Canada
  2. 2University of Toronto, Toronto, Ontario, Canada
  3. 3University Health Network Toronto Rehabilitation Institute, Toronto, Ontario, Canada
  1. Walter Swardfager, Department of Pharmacology & Toxicology, University of Toronto, 1 King’s College Circle, Toronto, Ontario, M5S 1A8, Canada. Email: w.swardfager@utoronto.ca

Abstract

Background. Ten percent of stroke survivors develop dementia, which increases to more than a third after recurrent stroke. Other survivors develop less severe vascular cognitive impairment. In the general population, depression, and diabetes interact in predicting dementia risk, and they are both prevalent in stroke. Objective. To assess the cumulative association of comorbid depressive symptoms and type 2 diabetes with cognitive outcomes among stroke survivors. Methods. Multicenter observational cohort study of people within 6 months of stroke. Depression and cognitive status were screened using the Center for Epidemiological Studies Depression (CES-D) scale and the Montreal Cognitive Assessment (MoCA), respectively. Processing speed, executive function and memory were assessed using the Trail Making Test parts A and B, and the 5 Word Delayed Free Recall task. Results. Among 342 participants (age 67.0 ± 13.5 years, 43.3% female, 46 ± 35 days poststroke), the prevalence of type 2 diabetes was 32.2% and depressive symptoms (CES-D ≥16) were found in 40.6%. Diabetes and depressive symptoms increased the risk of severe cognitive impairment (MoCA <20) with adjusted odds ratio (OR) 2.12 (95% confidence interval [CI] 1.20-3.74, P = .010) for 1 comorbidity and OR 3.18 (95% CI 1.26-8.02, P = .014) for both comorbidities. Associated cognitive deficits included executive function (F1, 168 = 3.43, P = .035) but not processing speed (F1, 168 = 1.86, P = .16) or memory (F1, 168 = 0.82, P = .44). Conclusions. Diabetes and depressive symptoms were associated cumulatively with poorer cognitive screening outcomes poststroke, particularly deficits in executive function. Having 1 comorbidity doubled the odds of screening for severe cognitive impairment, having both tripled the odds.

20 Must-Know Facts to Harness Neuroplasticity and Improve Brain Health

But absolutely nothing specific or even remotely close to a protocol. You are once again completely on your own with zero help from your medical team. I know this is a BHAG(Big Hairy Audacious Goal) .
But I don't fucking care how difficult it is, leaders tackle the difficult tasks. We have NO stroke leaders, you're screwed once again. Along with your children and grandchildren.
http://www.creativitypost.com/science/20_must_know_facts_to_harness_neuroplasticity_and_improve_brain_health
  1.  There is more than one “It” in “Use It or Lose It” -- our performance depends on a variety of brain functions and cognitive skills, not just one (be it "attention" or "memory" or any other).
  2.  Genes do not determine the fate of our brains. Thanks to lifelong neuroplasticity, our lifestyles are as important as our genes--if not more-- in how our brains grow and our minds evolve.
  3.  We need to pay more attention to Randomized Controlled Trials (RCTs) to verify whether any intervention causes an effect, and under what specific circumstances -- The media is doing quite a poor job, in our view, to educate the general public.
  4.  The largest recent RCT (the ongoing FINGER study) and a 2010 systematic review of all relevant RCTs provide useful guidance: First, they report a protective effect of social and cognitive engagement, physical exercise, and the Mediterranean diet. Second, the average benefits at the population level appear quite limited, so we need to have realistic expectations.
  5.  Physical exercise and increased fitness promote brain functioning through a variety of mechanisms, including increased brain volume, blood supply and growth hormone levels.
  6.  Cardiovascular exercise that gets the heart beating – from walking to skiing, tennis and basketball – seems to bring the greatest brain benefits; thirty to sixty minutes per day, three days a week, seems to be the best regimen.
  7.  Mental stimulation strengthens the connections between neurons (synapses), improving neuron survival and cognitive functioning. Mental stimulation also helps build cognitive reserve, helping the brain better cope with potential AD pathology.
  8.  Routine activities do not challenge the brain. Keeping up the challenge requires going to the next level of difficulty, or trying something new.
  9.  The only leisure activity that has been associated with reduced cognitive function is watching television.
  10.  Brain training can work, putting the "cells that fire together wire together" to good use, but available RCTs suggest some key conditions must be met to transfer to real-life benefits.
  11.  The brain needs a lot of energy: It extracts approximately 50% of the oxygen and 10% of the glucose from arterial blood.
  12.  The Mediterranean Diet, supplemented with olive oil and nuts, is associated with decreased risk of cognitive decline.
  13.  Moderate doses of caffeine increase alertness but there is no clear sustained lifetime health benefit (or harm).
  14.  Light-to-moderate alcohol consumption seems to lower the risk of dementia.
  15.  Taking "brain supplements" of any kind does not seem to boost cognitive function or reduce risks of cognitive decline or dementia, unless directed to address an identified deficiency.
  16.  The larger and the more complex a person’s social network is, the bigger the amygdala (which plays a major role in our behavior and motivation). There is no clear evidence to date on whether "online" relationships are fundamentally different from "offline" ones in this regard.
  17.  Chronic stress reduces and can even inhibit neurogenesis. Memory and general mental flexibility are impaired by chronic stress.
  18.  There is increasing evidence that meditation and biofeedback can successfully teach users to self-regulate physiological stress responses.
  19.  We will not have a Magic Pill or General Solution to solve all our cognitive challenges any time soon, so a holistic multi-pronged approach is recommended, centered around nutrition, stress management, and both physical and mental exercise.
  20.  Having said that, no size fits all, so it's critical to understand and address individual needs, priorities and starting points.

Wednesday, June 29, 2016

Red wine ice cream floats are a thing and obviously we need one RIGHT NOW

Ask for this during your hospital stay, say research has proven its benefits. Is their hospital so fucking far behind the times they haven't heard about this? That answer will prove how incompetent your stroke hospital is. Do you really want to be in an incompetent hospital?

All the great things studies claim drinking red wine can do:

1. Lower the risk of breast cancer.
2. Raise levels of good HDL cholesterol.
3. Be equivalent to an hour of exercise.
3. Give you better sleep quality.
4. Prevent tooth decay.
5. Reduce plaque in your arteries.
6. Make you have fewer colds.
7. Help you lose weight.
8. Lower your risk of heart disease, stroke, and dementia.
9. Give you "gorgeous skin."
10. Aid digestion.
11. Enhance exercise performance.
12. Control Type 2 Diabetes.
13. Help you "chill out."
14. Reduce risk of depression.
15. Give you a longer life.
16. Increase diversity of bacteria in your gut.
17. Fight off cavities.
18. Stop bug bites.
 

https://www.yahoo.com/news/red-wine-ice-cream-floats-125919307.html
A red wine ice cream float
You guys, this is not a drill. BKW, a new restaurant in Brooklyn is offering a red wine ice cream float that combines equal parts red wine and cola with a scoop of gelato. It sounds ridiculously decadent and delicious. Life-changing, actually. Here’s the lowdown via Food & Wine:
They combined their one Old Vine Zinfandel with grapes harvested from Lodi, CA, cola and Mascarpone gelato from one of the best ice cream purveyors in NYC,  Il Laboratoria del Gelato, into one supreme, grown up float. The gelato is served in its own glass, while the wine and cola are served in a pitcher for the diner to pour as their will, so that the ice cream doesn’t melt.
Definitely adding this restaurant to our NYC dining bucket list.
But in the meantime, we think we’ll mix up our own version of this recipe — $2 Trader Joe’s wine and Breyer’s might not be quite as glamorous, but on a hot summer evening, it will do just fine.

Procalcitonin and Midregional Proatrial Natriuretic Peptide as Markers of Ischemic Stroke

Have your doctor explain this one to you. Does it affect your risk of stroke? Inquiring minds want to know.
http://stroke.ahajournals.org/content/47/7/1714.abstract

The Northern Manhattan Study

  1. Mitchell S.V. Elkind, MD, MS
+ Author Affiliations
  1. From the Department of Neurology, Columbia University College of Physicians and Surgeons, New York, NY (M.K., Y.P.M., M.S.V.E.); Department of Neurology, University Hospital of Zurich, Zurich, Switzerland (M.K.); Department of Biostatistics (M.C.P.) and Department of Epidemiology (M.S.V.E.), Mailman School of Public Health, Columbia University, New York, NY; Department of Internal Medicine and Laboratory Medicine, Medical University Clinic, Kantonsspital Aarau, Switzerland (B.M., A.H.); and Departments of Neurology (R.L.S.) and Public Health Sciences and Human Genetics (R.L.S.), Miller School of Medicine, University of Miami, Coral Gables, FL.
  1. Correspondence to Mira Katan, MD, MS, Department of Neurology, University Hospital of Zurich, Frauenklinikstrasse 26, 8091 Zurich, Switzerland. E-mail mira.katan@usz.ch

Abstract

Background and Purpose—Chronic infections and neuroendocrine dysfunction may be risk factors for ischemic stroke (IS). We hypothesized that selected blood biomarkers of infection (procalcitonin [PCT]), hypothalamic–pituitary–axis function (copeptin), and hemodynamic dysfunction (midregional proatrial natriuretic peptide [MRproANP]) are associated with incident IS risk in the multiethnic, urban Northern Manhattan Study (NOMAS) cohort.
Methods—A nested case–control study was performed among initially stroke-free participants. Cases were defined as first IS (n=172). We randomly selected controls among those who did not develop an event (n=344). We calculated Cox proportional hazards models with inverse probability weighting to estimate the association of blood biomarkers with risk of stroke after adjusting for demographic, behavioral, and medical risk factors.
Results—Those with PCT and MRproANP, but not copeptin, in the top quartile, compared with the lowest quartile, were associated with IS (for PCT adjusted hazard ratio [HR], 1.9; 95% confidence interval [CI], 1.0–3.8 and for MRproANP adjusted HR, 3.5; 95% CI, 1.6–7.5). The associations of PCT and MRproANP differed by stroke etiology; PCT levels in the top quartile were particularly associated with small vessel stroke (adjusted HR, 5.1; 95% CI, 1.4–18.7) and MRproANP levels with cardioembolic stroke (adjusted HR, 16.3; 95% CI, 3.7–70.9).
Conclusions—Higher levels of PCT, a marker of infection, and MRproANP, a marker for hemodynamic stress, were independently associated with IS risk. PCT was specifically associated with small vessel and MRproANP with cardioembolic stroke risk. Further study is needed to validate these biomarkers and determine their significance in stroke risk prediction and prevention.

How to keep your blood pressure under control

Pretty much totally generically fucking worthless. With nothing specific in here the blame can always be shifted to the patient. What we really need is a specific diet protocol that contains actual amounts for reductions in blood pressure.
These would be a good starting point:

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

Body Fat Is Associated With Reduced Aortic Stiffness Until Middle Age


Stiff arteries relax like younger blood vessels after taking alagebrium

I have started taking BRE, no clue if it is doing any good.

Black Raspberry Extract Increased Circulating Endothelial Progenitor Cells and Improved Arterial Stiffness in Patients with Metabolic Syndrome: A Randomized Controlled Trial 

Antihypertensive Effect of Fermented Milk Products Under the Microscope

Melatonin reduces blood pressure and tunes up disrupted circadian rhythms in the elderly

Study: Aged Cheese Lowers Blood Pressure

Must-Have Foods That Can Help Lower Blood Pressure Naturally

Dietary nitrate lowers blood pressure

8 Produce Picks For Better Blood Pressure

UEA research shows high protein foods boost cardiovascular health

The Acute Electrocortical and Blood Pressure Effects of Chocolate

Daily Consumption of Blueberries May Lower Blood Pressure

Reduce High Blood Pressure with Beet Juice

New research shows almonds reduce the risk of heart disease

Regular pomegranate juice administered to hypertensive patients causeda significant drop in blood pressure [26], a reduction in carotid plaque development [27] 

 

The latest worthless one here:

How to keep your blood pressure under control


High blood pressure or hypertension is a “silent killer” with few warning signs. About 70 million people -- 1 out of 3 adults -- are living with it, but only 52 percent have it under control. This stealth disease is a common risk factor for heart disease and stroke, two leading causes of death in the United States.
It is difficult to tell on your own if you have hypertension as it has few to no symptoms. The single most important step to take is to have your blood pressure checked regularly by a healthcare professional and always ask what it is so you know how it is doing.
What is blood pressure and why is it important?
Blood pressure is vital to life. It’s the force of blood against the walls of the arteries pushing blood through the major arteries into smaller arteries and finally into tiny capillaries allowing the exchange of fluids between the blood and tissues.
When our blood pressure is taken, two numbers are given such as 110/70. The top number is called the systolic pressure which is blood pressure at its highest when the heart is beating. The bottom number is called the diastolic pressure which is blood pressure when the heart is at rest or between beats and the pressure falls.
Throughout the day, blood pressure rises and falls but when it stays high for prolonged periods of time, this can damage the heart and raise your risk for a heart attack or stroke. When the force of blood flow is high, blood vessels stretch so blood flows more easily. Eventually, this stretching scars and weakens blood vessels throughout the body.
The kidneys, which help regulate blood pressure, can also be affected by hypertension. Uncontrolled high blood pressure can cause arteries around the kidneys to narrow, weaken, or harden making hypertension the second leading cause of kidney failure in the United States after diabetes.
Symptoms and causes
Most people do not have any symptoms of hypertension. Some people may experience headaches or nose bleeds but these usually don’t occur until severe hypertension is reached. That is why each time a person goes to a doctor, their blood pressure is always taken. Ideal resting blood pressure is 120/80 or lower. High blood pressure is defined as 140/90 or higher.
There are two types of hypertension: primary or essential hypertension and secondary hypertension
Primary hypertension is when there is no identifiable cause of high blood pressure. This type tends to develop over several years.
Secondary hypertension is caused by an underlying condition. It tends to appear suddenly and causes a higher reading than primary hypertension. Some conditions that can lead to secondary hypertension are kidney or thyroid problems, sleep apnea, or alcohol abuse.
  • Risk factors
    Age – Hypertension risk increases with age. More than two-thirds of adults over age 65 have it, and individuals who have a normal blood pressure at age 55, will have a 90 percent chance of developing high blood pressure during their lifetime.
  • Family history – High blood pressure tends to run in families.
  • Race – It is particularly common among African Americans and often develops at an earlier age than in Caucasians.
  • Obesity – It is estimated that 70 percent of people with hypertension are overweight or obese. Obesity raises blood pressure by altering kidney function, increasing blood volume, and promoting blood vessel damage through insulin resistance. Excess fat also means miles of extra capillaries through which the blood must be pumped.
  • High salt intake – As salt intake increases, so does blood pressure.
  • Reduced potassium intake – Potassium helps balance the amount of sodium in your cells. By not having enough potassium in your diet, too much salt can accumulate in the blood.
  • Alcohol – More than two drinks a day is strongly associated with hypertension. 
  • Stress – High stress can lead to increased blood pressure.
  • Certain chronic conditions – Having diabetes, kidney disease, or sleep apnea can raise blood pressure.
Complications
Uncontrolled hypertension can lead to several medical complications which can include:
  • Heart or stroke
  • Aneurysm
  • Heart failure
  • Weakened and narrowed blood vessels in your kidneys
  • Thickened, narrowed or torn blood vessels in the eyes
  • Metabolic syndrome
  • Trouble with memory or understanding
Lifestyle modifications to treat hypertension
Fortunately, there are many lifestyle modifications a person can make to either prevent or treat high blood pressure. The sooner in life one adopts these changes, the greater the likelihood they can avoid or reduce the risk of it developing to begin with.
Here are ways you can help reduce your high blood pressure:
  • Weight reduction – Maintain a healthy body weight (Body Mass Index or BMI of 18.5-24.9).
  • DASH eating plan – Adopt the DASH (Dietary Approaches to Stop Hypertension) diet rich in fruits, vegetables, and low-fat milk products with reduced saturated fat intake.
  • Sodium restriction – Reduce sodium intake to less than 2,300 milligrams of sodium per day and further reduce intake to 1,500 milligrams among people with prehypertension or hypertension for greater reductions in blood pressure.
  • Physical activity – Perform aerobic physical activity for at least 30 minutes per day, most days of the week.
  • Moderate alcohol consumption – Men: limit to 2 drinks per day; women: limit to 1 drink per day.
There are also several medications to treat hypertension. The category of medication your doctor may prescribe depends on your blood pressure measurements and other medical history.
 

Cutting-edge imaging technologies are being used to understand what causes muscle contracture after a stroke and how we can improve treatments.

The first studies I've seen that are looking into objectively describing contractures. This first step is required before we can even attempt to prevent it from happening. This come from Neuroscience Research Australia (NeuRA).
Page 29 for the stroke info:
https://www.neura.edu.au/neura-profile/2016/#28

Neuroscience Research Australia (NeuRA).
Neuroscience Research Australia (NeuRA).

I was super-fit - so why did I have a stroke at 35?

I was super fit at 50, Why did I have a stroke? Because my Dads' doctor did not tell him to have his children tested for blocked carotids when he was found to have 80% blockage. This notification should have rolled out to every cardiologist in the world, so it wouldn't happen again. So cardiologists seem to be as bad as neurologists in not talking to each other or have protocols to update.

I was super-fit - so why did I have a stroke at 35?

VA partners with IBM to use supercomputer Watson to treat cancer

Just when the fuck will our fucking failures of stroke associations ask IBM and Dr. Watson for help in solving all the problems in stroke? They already have proven they are not smart enough to solve even easy problems themselves mainly because they haven't even tried.  IBM is already engaged in other medical questions. WHY NOT STROKE?

IBM, Pfizer team on remote monitoring for Parkinson’s care - Why not stroke?

IBM Watson Health GM: Partnerships set us apart

IBM Watson, Boston Children’s team on rare pediatric diseases

IBM Starts New Precision Medicine Program - for cancer

Massive IBM deal gives Watson purpose and puts it in pole position to transform healthcare - What about stroke?

IBM's Watson Comes to the Bedside

Why And How Healthcare Institutions Should Prepare For IBM Watson

Pharma puts Watson brain to work to speed up R&D, cut drug development costs

IBM's Watson Supercomputer May Soon Be The Best Doctor In The World

MD Anderson Cancer Center to Use IBM Watson

IBM's Watson Does Drug Discovery?

 

 

 

 The latest here:

VA partners with IBM to use supercomputer Watson to treat cancer 

Cannabinoids remove plaque-forming Alzheimer's proteins from brain cells

I bet no matter what scientific proof is given our legislators will not remove marijuana from Schedule I classification. States will have to do it and drag our federal government kicking and screaming into a new world. Stroke survivors will likely need this due to our increased chances of getting dementia/Alzheimers.
http://medicalxpress.com/news/2016-06-cannabinoids-plaque-forming-alzheimer-proteins-brain.html
Salk Institute scientists have found preliminary evidence that tetrahydrocannabinol (THC) and other compounds found in marijuana can promote the cellular removal of amyloid beta, a toxic protein associated with Alzheimer's disease.
While these exploratory studies were conducted in neurons grown in the laboratory, they may offer insight into the role of inflammation in Alzheimer's disease and could provide clues to developing novel therapeutics for the disorder.
"Although other studies have offered evidence that cannabinoids might be neuroprotective against the symptoms of Alzheimer's, we believe our study is the first to demonstrate that cannabinoids affect both inflammation and amyloid beta accumulation in nerve cells," says Salk Professor David Schubert, the senior author of the paper.
Alzheimer's disease is a progressive brain disorder that leads to memory loss and can seriously impair a person's ability to carry out daily tasks. It affects more than five million Americans according to the National Institutes of Health, and is a leading cause of death. It is also the most common cause of dementia and its incidence is expected to triple during the next 50 years.
It has long been known that amyloid beta accumulates within the nerve cells of the aging brain well before the appearance of Alzheimer's disease symptoms and plaques. Amyloid beta is a major component of the plaque deposits that are a hallmark of the disease. But the precise role of amyloid beta and the plaques it forms in the disease process remains unclear.
In a manuscript published in June 2016's Aging and Mechanisms of Disease, Salk team studied nerve cells altered to produce high levels of amyloid beta to mimic aspects of Alzheimer's disease.
The researchers found that high levels of amyloid beta were associated with cellular inflammation and higher rates of neuron death. They demonstrated that exposing the cells to THC reduced amyloid beta protein levels and eliminated the from the nerve cells caused by the protein, thereby allowing the nerve cells to survive.
"Inflammation within the brain is a major component of the damage associated with Alzheimer's disease, but it has always been assumed that this response was coming from immune-like cells in the brain, not the nerve cells themselves," says Antonio Currais, a postdoctoral researcher in Schubert's laboratory and first author of the paper. "When we were able to identify the molecular basis of the inflammatory response to amyloid beta, it became clear that THC-like compounds that the nerve cells make themselves may be involved in protecting the cells from dying."
Brain cells have switches known as receptors that can be activated by endocannabinoids, a class of lipid molecules made by the body that are used for intercellular signaling in the brain. The psychoactive effects of marijuana are caused by THC, a molecule similar in activity to endocannabinoids that can activate the same receptors. Physical activity results in the production of endocannabinoids and some studies have shown that exercise may slow the progression of Alzheimer's disease.
Schubert emphasized that his team's findings were conducted in exploratory laboratory models, and that the use of THC-like compounds as a therapy would need to be tested in clinical trials.
In separate but related research, his lab found an Alzheimer's drug candidate called J147 that also removes amyloid beta from nerve cells and reduces the inflammatory response in both and the brain. It was the study of J147 that led the scientists to discover that endocannabinoids are involved in the removal of amyloid beta and the reduction of inflammation.
More information: Antonio Currais et al. Amyloid proteotoxicity initiates an inflammatory response blocked by cannabinoids, npj Aging and Mechanisms of Disease (2016). DOI: 10.1038/npjamd.2016.12

Stroke Treatment and Recovery. Are You Serious?

Everything here should be publicly available to all therapists and survivors with protocols explaining how they work and their efficacy.  That is what a great stroke association would do rather than hiding it in individual practices. Or having survivors on the do-it-yourself hunt for therapy that works.
http://www.neurorehabdirectory.com/stroke-treatment-recovery-serious/
It is true that recovering from a stroke will be an uphill battle for many, however, it is also accurate that the latest research findings regarding neuro recovery are more promising than ever before. How serious are you with embracing evidence into your practice? As a clinician, are you stuck using numerous theoretical-based treatment concepts that have not scientifically been proven to be effective?
Listed below are some of the common interventions supported by research that have shown positive results. How many of the below techniques are in your current therapy toolbox? (Who gives a shit what is in the toolbox? WHAT ARE YOUR RESULTS YOU FUCKING IDIOTS)If just a few, then why?


Arm and Hand Research Findings


Mobility and Leg Research Findings


Vision Recovery Research Findings

  • Computer-based scanning therapy, such as Visual Motor Training and Virtual Reality/Exercise Games can improve visual neglect.
  • Wearing Visual Aids, like Prisms, may improve functional performance with every-day tasks. Prisms can be used to reduce the apparent visual field loss by shifting visual stimuli from the blind field into the patient’s seeing field. These prisms are fitted to glasses but need to be restricted to just one half of each of the lenses (typically on the side of the blind field).
  • Visual scanning techniques can improve visual neglect with associated improvements in function.
  • Compensatory training (adapting to the vision loss) can significantly improve search performance and efficiency.

Search By Product Category

Arm Bike
An Arm is a stationary cycle designed to strengthen and condition the upper body, as well as the cardiovascular system, by using the arms.
Biofeedback
Biofeedback or electromyography (EMG) is a non-invasive technique used for measuring muscle electrical activity that occurs during muscle contraction and relaxation.
Body Weight Support
Body Weight Support uses a suspension system and a harness to support a percentage of the user’s body weight during standing, walking or exercise.
Electrical Stimulation
Electrical stimulation or neuromuscular electrical stimulation (NMES) is a technique used to elicit a muscle contraction using electrical impulses. Electrical current is then sent from the unit to the electrodes and delivered into the muscle causing a contraction.
EMG-Triggered Stimulation
EMG-Triggered Stimulation is based on the user’s voluntary movement, or intent to move. Electrodes, controlled by a unit, are placed on the skin over a specific area. Once the user attempts to contract his or her muscles and reaches the prescribed threshold, stimulation is triggered (delivered) to the same muscles. Various visual and auditory feedback options monitor the progress.
Exercise Aid
An Exercise Aid is a piece of equipment used during physical activity to improve strength and coordination of the body region targeted.
Foot Drop Brace
A Foot Drop Brace is a rigid or flexible support that offers dynamic or static assistance to the weakened foot so functional mobility and exercises can be possible.
Hand Function Splint
A Hand Function Splint is a rigid or flexible brace that offers dynamic or static assistance to the weakened hand so functional activities and exercises can be possible.
Leg Bike
A Leg Bike is a stationary cycle designed to strengthen and condition the lower body, as well as the cardiovascular system, by using the legs.
Lower Limb Robot-Assisted Therapy
Lower Limb Robot-Assisted Therapy consists of an electromechanical device, designed for the leg, that is used to assist users (through powered mobility) with exercise training and activities of daily living (ADL).
Mirror Therapy
In Mirror Therapy, a mirror is placed beside the unaffected limb, blocking the view of the affected limb. This creates the illusion that both limbs are functioning properly. Damaged areas of the brain’s motor cortex may improve by viewing movements of intact, functioning limbs.
Mobile Arm Support
A Mobile Arm Support (MAS) is a gravity supported mechanical device mounted on wheelchairs, tables, or base frames. A MAS is used to support the weak arm to improve motor function and strength. In addition, the device allows patients with shoulder weakness to perform self care tasks such as feeding, hygiene, grooming, and writing.
Shoulder Subluxation Sling
A Subluxation Sling is typically used on hemiparetic arms that are flaccid or exhibit minimal to no movement. They offer support, protection against injury and can prevent or reduce shoulder pain.
Upper Limb Contracture Splint
A Upper Limb Contracture Splint is a brace used to prevent or treat contractures. The goal of a contracture splint is to help keep the soft tissues (muscle and tendons) in the arm and hand stretched properly.
Upper Limb Robot-Assisted Therapy
Upper Limb Robot-Assisted Therapy consists of an electromechanical device, designed for the arm or hand, that is used to assist users (through powered mobility) with exercise training and activities of daily living (ADL).

Vegetarian diet: A prescription for high blood pressure? A systematic review of the literature

You can have your doctor look at this but I highly doubt it is going to tell you that eating 5 oz. of some specific food daily will reduce your blood pressure by x points. That is what is needed(a protocol) and I don't see anyone addressing that need. Everyone is just doing their conscience laundering by suggesting generic stuff.
http://www.mdlinx.com/internal-medicine/medical-news-article/2016/06/29/diet-high-blood-pressure-hypertension-nonvegetarian/6737090/?
The Journal for Nurse Practitioners , 06/29/2016
Hypertension is a standout amongst the most costly and poorly treated medical conditions in the United States and around the globe. Results of hypertension incorporate morbidity and mortality identified with its long–term impacts, which incorporate stroke, myocardial infarction, renal failure, limb loss, aortic aneurysm, and atrial fibrillation, among numerous others. In spite of the fact that there is an armamentarium of drugs to treat hypertension, they do little for avoidance. In this study they inspect the relationship amongst vegetarian and non–vegetarian diets and the pervasiveness of hypertension.
Go to Abstract Print Article Summary Cat 2 CME Report

The Body's Grace: Insights from a Paralyzed Yoga Teacher

I tried to get in one of his classes. I went to a regular yoga class for a while, the assumption was made that you knew yoga terms before starting, not true in my case. While I could do a lot of the poses they usually required me to see them first and figure out a way modify them to work for me. Matthew Sanford would be going a lot slower. The tai chi class I went to was much better.

The Body's Grace: Insights from a Paralyzed Yoga Teacher

"Matthew Sanford says he's never seen anyone live more deeply in their body -- in all its grace and all its flaws -- without becoming more compassionate toward all of life. He's a renowned teacher of yoga. And he's been paralyzed from the chest down since a car accident in 1978, when he was 13. He teaches yoga to the able-bodied. He also adapts yoga for people with ailments and disabilities, including military veterans. But Matthew Sanford has wisdom for us all on the strength and grace of our bodies, as we move through the ordinary span of our lives." { read more }

Tuesday, June 28, 2016

Advances in Our Knowledge of Stroke Mechanisms and Therapy

I can't say that this has advanced my knowledge one bit.
http://www.dana.org/Publications/ReportOnProgress/Advances_in_Our_Knowledge_of_Stroke_Mechanisms_and_Therapy/

Xuefang Ren, M.D.
Department of Physiology and Pharmacology
Experimental Stroke Core, Center for Basic and Translational Stroke Research
West Virginia University
James W. Simpkins Ph.D. (Report on Progress June 2016)James W. Simpkins, Ph.D.
Department of Physiology and Pharmacology
Experimental Stroke Core, Center for Basic and Translational Stroke Research
West Virginia University


View Article as PDF

Stroke, the most common medical emergency, is a cerebrovascular accident that can cause death and long-term disability. Over 80 percent of all strokes are ischemic strokes, when a clot lodges in an artery supplying blood to the brain and the blood flow is reduced or blocked. A small percentage, caused by rupture of brain blood vessels, are called hemorrhagic strokes. Stroke risk factors are well known and include high blood pressure, elevated lipids, diabetes, smoking, heavy drinking, coronary artery disease, heart diseases, etc.
Both ischemic and hemorrhagic strokes may cause a variety of neurologic symptoms, including sudden death, loss of consciousness, one-sided numbness, weakness, paralysis, sudden deafness, visual impairment, or difficulty in speaking, thinking, or understanding speech. Specific symptoms correspond with the location of stroke injury. For example, stroke damage in the brain stem (a pivotal center in the regulation of cardiac and respiratory function) may cause sudden death; a clot or bleeding in middle cerebral artery (MCA) territory (including the motor cortex and the underlying caudate-putamen), may cause numbness, weakness or paralysis of the contralateral side of the body.

A computerized tomography (CT) scan or Magnetic Resonance Imaging (MRI) is required to distinguish ischemic and hemorrhagic strokes. One of these images is required for clinicians to decide on the therapeutic strategies for patients when a stroke occurs. There are different mechanisms and treatments for ischemic and hemorrhagic strokes. Here we focus on the description of our current knowledge of the mechanisms and current treatments for ischemic stroke.
Current Treatments
A stroke requires immediate medical attention and urgent care because stroke damage to the brain evolves every second. To date, intravenous thrombolytic agents (which pharmacologically dissolve clots) and surgical strategies (which retrieve clots by mechanical means) are used to treat acute ischemic stroke. Tissue plasma activator (tPA) is the only FDA approved medication for acute ischemic stroke and must be used within 4.5 hours from the time of the onset of symptoms of stroke. Other medical thrombolytic drugs such as streptokinase and aspirin, show higher mortality or disability, and a higher risk of brain hemorrhage. Surgical interventions should be performed within 6 hours of acute stroke symptoms, and only after a patient receives tPA. Considerable improvements in stroke outcome are seen with both tPA and surgical clot removal when used within their allowable time windows.

Mechanisms in Ischemic Stroke

Experimental animal stroke models and cell culture models were developed for stroke studies several decades ago and rigorous scientific investigations have been undertaken. Some models mimic pathophysiological changes in human stroke and address many puzzles in understanding stroke mechanisms, which are essential in developing effective therapeutic strategies for stroke patients.

Figure 1 describes our current understanding of stroke mechanism: during the first few hours, the primary ischemic stroke injury is due to the occlusion of the blood vessels. The occlusion leads to an insufficient energy supply to the brain tissue and causes neuronal death and neurological damage. Reduced oxygen supply compromises mitochondrial function and causes anaerobic glycolysis (transforms glucose to lactic acid when an insufficient amount of oxygen is available). Elevated levels of lactic acid make the brain tissue acid and results in decreased ATP production and reduced ion pumps activity on cell membrane. As a consequence, concentrations of protons, calcium, and sodium ions increase in the cells. This results in water influx into the cells, cell swelling, death, and formation of core infarction in primary stroke injury. This series of events evolve quickly in the primary stroke site, but might be salvageable by treatment within minutes to hours. Secondary stroke damage is initiated by post-stroke disruption of the blood-brain barrier (BBB), initiating a cascade damaging molecular processes. BBB is formed by endothelial cells surrounding the brain’s vasculature, which restrict access of molecules in the general circulation of the brain (See Figure 1 and following text).
Report on Progress - Advances in Our Knowledge of Stroke Mechanisms and Therapy - Figure1 (Click on image to view larger)
Figure 1. Mechanisms in Ischemic Stroke Damage.Ischemia causes immediate brain damage in primary stroke injury and delayed brain damage in secondary stroke injury. Mitochondrial failure plays a critical role in BBB opening that involves in vascular edema following stroke.
Mitochondrial failure and BBB disruptionBBB opening is a key stage in secondary stroke injury and has been linked to increased stroke damage and vascular edema in animal models of stroke. Several groups have observed a biphasic BBB breakdown after transient stroke in animal models. The first BBB disruption occurs within several hours of the onset of ischemia and a second phase of BBB opening may happen after several days of ischemia. Recently, using an experimental model of stroke, our group has shown that mitochondria play a critical role in the first BBB opening1. Due to lack of oxygen, mitochondrial failure decreases ATP production in the endothelial cells surrounding the blood vessels in the brain, causing a breakdown of the BBB and further exacerbating stroke damage2.
We have also shown that lipopolysaccharide (LPS, an exotoxin extracted from bacteria and used to mimic bacterial infection) worsens stroke outcomes by the same mechanisms of compromised mitochondria in the endothelial cells1-3. We have also found that a food preservative, tBHQ, interferes with mitochondrial function and worsens stroke outcome as well4. This evidence suggests that mitochondrial dysfunction plays a critical role in the first BBB disruption and acute stroke damage.
It is not known yet how the BBB is repaired after the initial first opening. There is a debate as to whether the second BBB opening contributes to brain damage or brain repair after stroke. More investigation is need to resolve this issue.
Reactive oxygen species (ROS) and stroke5About 95 percent of ROS, such as superoxide (O2•−) and hydrogen peroxide (H2O2) are derived from electron leakage during the activity of the mitochondrial respiratory chain, which generates ATP. These ROS are scavenged by manganese-superoxide dismutase (Mn-SOD or SOD2), catalase and glutathione peroxidase. Ischemic stress triggers a disturbance of the mitochondrial membrane potential and the normal proton gradient, which results in excessive ROS generation via electron transfer for the ATP synthesis.
The overproduction of ROS overwhelms oxidant scavenging capacity and establishes a vicious positive feedback loop in which increased ROS-induced ROS production. ROS also damage mitochondrial DNA, induce activation and secretion of matrix metalloproteinases (MMPs), activate inflammatory responses, and lead to cell swelling and death. This process causes BBB damage and secondary injury in acute stroke. However, ROS may also be involved in tissue remodeling and angiogenesis (new blood vessel formation) in the late phase of stroke.
Matrix metalloproteinases (MMPs) and stroke6MMPs, a large family of proteolytic enzymes, are present in various cells in latent forms and are capable of degrading all components of the extracellular matrix. ROS may induce activation and secretion of MMP-2 in astrocytes, MMP-3 and MMP-9 in endothelial cells and in neutrophils. The activated MMPs breakdown and degrade tight junctions, a critical component of the BBB, and contribute to BBB disruption and hemorrhagic transformation in acute stroke. Interestingly, evidence also suggest that MMPs participate in brain repair in the stroke late phase.

Inflammatory responses in the ischemic brain
7
Our immune system protects the body from infections. We did not anticipate that the immune system would play a negative role in stroke by attacking brain tissue as it were “foreign”. However, this does happen in most of cases of acute strokes. Inflammatory responses are initiated in the clots causing the stroke. Platelets and white blood cells (WBCs) are trapped in the clot fibrin due to hypoxia and shear stress in small blood vessels. MMPs are released by leukocytes and facilitate the BBB opening. Following the BBB disruption, neutrophils, lymphocytes, and monocytes from peripheral blood infiltrate into the brain tissue. Pro-inflammatory cytokinesand chemokine released by WBCs may destroy brain neurons directly or indirectly. The inflammatory cells currently being actively investigated include:
NeutrophilsNeutrophils, an essential part of the innate immune system, are one of the first peripheral responding WBCs to launch a defense against all classes of infections. Vesicles that contain various enzymes, including oxidase and MMPs are stored in neutrophils. Hypoxia induces the secretion of chemokines by neurons, which attract the migration of neutrophils; meanwhile hypoxia-induced ROS over-production activates the release of the MMPs from neutrophils that can attack BBB, permitting neutrophils to migrate into the ischemic brain tissue via the degraded BBB. From there, neutrophils phagocytose dying neurons and release a large amount of granules and ROS that may kill both dying and living neurons.

Antigen Presentation Cells (APCs)APCs are classified as professional APCs and non-professional APCs. The former includes macrophages, microglia, dendritic cells, B cells, and monocytes. From our basic immunology book, we know that professional APCs express major histocompatibility complex II (MHCII) on their surfaces and present antigens to T-cells. Non-professional APCs express MHC class 1 molecules on their surface. Following BBB disruption and the release of brain antigens into the periphery, these APCs present brain antigens to T-cells in the late stage of ischemic stroke, and they may be partially responsible for ischemia-induced dementia. However, in acute stroke, APCs may produce pro-inflammatory cytokines, such as TNF-α and IL-1β that contribute to post-stroke inflammation; they may also produce anti-inflammatory cytokines IL-10 and TGF-β, which promote healing and reduce inflammatory responses.
LymphocytesLymphocytes, including T-cells and B-cells belong to the adaptive immune system that involves both cellular and humoral immunity against antigens. Growing evidences indicate that T-cells and B-cells participate in the progression of ischemic stroke. Elevated antibodies (produced by B-cells) against brain antigens, and increased cytokines (secreted by T-cells and other WBCs) are detected in stroke, suggesting cellular and humoral responses to ischemic brain damage. Using the experimental stroke animal model, we have previously demonstrated that B-cells are protective in acute strokes .by secreting anti-inflammatory cytokine IL-10. Another group found that B-cells could impair cognitive behavioral outcomes and contribute to post-stroke dementia in the late phase.
Researchers are striving to identify the role of T cells in stroke. Tolerated T-cells that induce a TH2 cytokine response, including IL-4 and IL-10 secretion, reduce stroke infarction. TH1 cells, secreting pro-inflammatory cytokines (such as IL-1beta, TNF-alpha, and IFN-gamma,) exacerbate stroke. Mice, which have the recombination activation gene (RAG1) inactivated are deficient in T-cells and B-cells and are protected from ischemia. However, transfer of naive T-cells worsens stroke infarction following 24 hours reperfusion, suggesting that T-cells are detrimental early in stroke. It has been demonstrated that γδT cells (a unique T-cell subtype that links adaptive and innate immune system) contribute to brain damage by secreting a pro-inflammatory cytokine IL-17.
Other mechanismsScientists have also investigated other mechanisms in stroke, such as, glutamate and other excitatory neurotransmitters released by dying neurons which cause exotoxic damage to healthy neurons. MicroRNAs, a hot topic in life sciences, are changed in stroke animals and patients, and might be involved in brain damage and recovery as well. Other studies have also revealed that nitric oxide (NO) and peroxynitrite (ONOO−) produced simultaneously with superoxide in stroke, are detrimental to brain neurons.
Future perspectivesDespite the benefits afforded by tPA and surgical treatments, there is a desperate need to develop more effective therapies for stroke because very few stroke patients can meet the brief time window necessary for effective clot removal. While there are still debates as to whether we have successfully traveled from clot removal in early stroke to effective treatments in the second stroke injury, it is clear that we have gained more knowledge in the past two decades than any in our prior history. The failure of several clinical trials on some potential drugs raises questions about our complete understanding of the mechanisms in stroke. Given the complicated mechanisms revealed so far, drugs that target a single mechanism may not be able to stop the progression of post-stroke injury. However, if properly timed, we believe that preserving mitochondrial function in the BBB might be able to restrict the damage of stroke. We anticipate that a cocktail of compounds will be needed to preserve mitochondrial function representing a novel strategy for stroke treatments.
Further reading
1. Doll, D. N. et al. Mitochondrial crisis in cerebrovascular endothelial cells opens the blood-brain barrier. Stroke; a journal of cerebral circulation46, 1681-1689, doi:10.1161/STROKEAHA.115.009099 (2015).
2. Hu, H. et al. Mitochondrial Impairment in Cerebrovascular Endothelial Cells is Involved in the Correlation between Body Temperature and Stroke Severity. Aging and disease7, 14-27, doi:10.14336/AD.2015.0906 (2016).
3. Doll, D. N. et al. Lipopolysaccharide exacerbates infarct size and results in worsened post-stroke behavioral outcomes. Behavioral and brain functions : BBF11, 32, doi:10.1186/s12993-015-0077-5 (2015).
4. Sun, J., Hu, H., Ren, X. & Simpkins, J. W. Tert-butylhydroquinone compromises survival in murine experimental stroke. Neurotoxicology and teratology54, 15-21, doi:10.1016/j.ntt.2016.01.004 (2016).
5. Kalogeris, T., Bao, Y. & Korthuis, R. J. Mitochondrial reactive oxygen species: a double edged sword in ischemia/reperfusion vs preconditioning. Redox biology2, 702-714, doi:10.1016/j.redox.2014.05.006 (2014).
6. Turner, R. J. & Sharp, F. R. Implications of MMP9 for Blood Brain Barrier Disruption and Hemorrhagic Transformation Following Ischemic Stroke. Frontiers in cellular neuroscience10, 56, doi:10.3389/fncel.2016.00056 (2016).
7. Iadecola, C. & Anrather, J. The immunology of stroke: from mechanisms to translation. Nature medicine17, 796-808, doi:10.1038/nm.2399 (2011).
8. Doll, D. N., Rellick, S. L., Barr, T. L., Ren, X. & Simpkins, J. W. Rapid mitochondrial dysfunction mediates TNF-alpha-induced neurotoxicity. Journal of neurochemistry132, 443-451, doi:10.1111/jnc.13008 (2015).