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 481 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

Sunday, February 14, 2016

The Most Reassuring Thing You Can Say To Someone Experiencing Fear And Anxiety

Is your doctor using this to diffuse your fear and anxiety about not recovering because they have no stroke protocols to get you 100% recovered?

The Most Reassuring Thing You Can Say To Someone Experiencing Fear And Anxiety

Persevere, and the fear will dissolve.

Depression after a stroke can be successfully treated

Articles like this need to be responded to because the doctors writing them are not looking at cause and effect. They are looking at current rehab rather than future possibilities if they would only solve all the fucking problems in stroke. People like this that don't look ahead are not leaders.
My response was:
Depression wouldn't be so bad if our doctors/researchers would stop the neuronal cascade of death. Thus resulting in vastly less disability. I know that Dr. Tymianski has talked about 1000+ neuroprotective trials that have failed. That is no reason to give up. There are only 5 currently known causes to solve:
1. glutamate poisoning
2. excitotoxicity
3. Capillaries that don't open due to pericytes
4. Inflammatory action leaking through the blood brain barrier.
5. Lysosomal Membrane Permeabilization as a Key Player in Brain Ischemic Cell Death

http://www.dailyherald.com/article/20160213/entlife/160219936/#articlecomments 
Q: My mother had a stroke that weakened one side of her body. But the bigger problem right now is her depression. Can that be treated, or is it caused by irreversible brain damage from the stroke?
A: Strokes can cause significant problems. People can have difficulty moving (like your mother). They can have trouble speaking or understanding speech. They can have trouble thinking. Being suddenly hit with any or all of those losses would depress anyone -- including people who never suffered from depression before.
About one in four people who've had a stroke develop major depression. In part, this is a reaction to the terrible losses caused by a stroke. But you're right that the injury to the brain from the stroke can itself cause changes in brain chemistry that lead to depression.
In other words, depression following a stroke can be similar to depression following another major illness that affects a person's life but does not injure the brain -- such as a heart attack or cancer. But it also can be caused by the brain injury itself.
You might think that in someone who has difficulty talking or understanding speech, or difficulty moving her arms and legs, depression is the least of her problems. But the mental anguish of depression isn't a minor concern.
Left untreated, depression can undermine efforts at rehabilitation and worsen cognitive disabilities.
Depression after a stroke is associated with poorer outcomes a year after the stroke has occurred. It's also associated with a higher death rate in subsequent years.
Fortunately, antidepressants seem to be fairly effective. In 2008, scientists published a review of the research in this area. They concluded that the medications had a "small but significant" effect on post-stroke depression.
What's more, the benefits of antidepressants may not be limited to relieving depression; they may positively affect areas and networks in the brain that improve other impaired functions as well. Studies have found that certain antidepressants, in combination with physical therapy, can help with recovery from stroke-induced paralysis, muscle weakness and overall disability.
If you haven't already done so, talk to your mother's doctor about her depression. Ask the doctor to recommend a psychiatrist who has experience working with stroke patients, or find out if there is a mental health professional affiliated with your mother's rehab program.
Treatment of stroke has improved greatly in this country. Some people who would have died or been severely disabled can now do quite well. That's due, in part, to powerful drugs that can quickly open blocked blood vessels in the brain.
More recently, stents that grasp and remove the blood clots that are blocking blood flow to the brain have been found to be effective. They more than double the chance that a patient with a stroke will become functionally independent.
Doctors who concentrate on deploying all of these new treatments available for patients with stroke can sometimes neglect to recognize and treat depression. If you think that might be happening with your mother, raise that issue with her doctor.
• Dr. Anthony Komaroff is a physician and professor at Harvard Medical School. To send questions, go to AskDoctorK.com, or write: Ask Doctor K, 10 Shattuck St., Second Floor, Boston, MA 02115.

Why it’s good to be lonely this Valentine’s Day

Well I am alone but not lonely, movies tonight with a friend, 'Kingsman'.
http://www.alphagalileo.org/ViewItem.aspx?ItemId=138979&CultureCode=en
Whilst it may seem that there are no positives to draw from feeling lonely, several authors have shown that this is not the case.
In the article ‘Evolutionary mechanisms for loneliness’, from the journal Cognition & Emotion, authors John T. Cacioppo, Stephanie Cacioppo & Dorret I. Boomsma explore how people in ‘happy’ relationships negatively view the lonely but suggest that loneliness in fact promotes an individual’s genetic survival.
The authors report that the ‘lonely’ are viewed more negatively in terms of their psychosocial functioning and attractiveness. In a social environment non-lonely people form a negative impression towards lonely people, which then affects their behaviour and reinforces the lonely individual’s perceived isolated existence. Furthermore, individuals rated opposite-gender partners who they expected to be lonely as less sociable, and behaved towards them in a less sociable manner than they did toward partners they expected not to be-lonely.
But despite the negativity towards lonely people, there is good news for those feeling glum this Valentine’s Day. Although it may feel like loneliness has no redeeming features, it promotes behavior change to increase the likelihood of the survival of one’s genes.
Therefore loneliness is not so much a dysfunctional reaction as it is about promoting an individual’s genetic legacy.
*Read the full article online
http://www.tandfonline.com/doi/full/10.1080/02699931.2013.837379#.UvilEPl_v_M

Researchers develop a 'super-spaghetti' with healthy properties which lessens the risk of suffering cardiovascular diseases

How many decades will it take before this shows up in your hospital diet?
http://www.mdlinx.com/internal-medicine/top-medical-news/article/2016/02/02/11

University of Granada Health Science and Technology News
Researchers from the University of Granada and from the Research and Development of Functional Food Centre, along with two Italian universities, have developed a pasta enriched in fibre and antioxidants, elaborated with functional flours, in a project partially funded by the CEI BioTic centre. A single dish of this pasta contributes to 70% of the daily dose of betaglucans recommended by the European Food Safety Authority.

Regular caffeine consumption does not result in extra heartbeats, study shows

See how long it takes before your doctor tells you about this.
http://www.mdlinx.com/internal-medicine/top-medical-news/article/2016/02/02/3
Contrary to current clinical belief, regular caffeine consumption does not lead to extra heartbeats, which, while common, can lead in rare cases to heart– or stroke–related morbidity and mortality, according to UC San Francisco researchers. The study, which measured the chronic consumption of caffeinated products over a 12–month period, rather than acute consumption, appears in the January 2016 issue of the Journal of the American Heart Association. It is the largest to date to have evaluated dietary patterns in relation to extra heartbeats.

Natural protein points to new inflammation treatment

Would this be useful in fighting the inflammation in our arteries? We'll never know because our fucking failures of stroke associations do not followup any promising research.
http://www.mdlinx.com/internal-medicine/top-medical-news/article/2016/02/08/3
Findings may offer insight to effective treatments for inflammatory diseases, such as rheumatoid arthritis, psoriasis, and multiple sclerosis.
Increasing the level of a naturally–produced protein, called tristetraprolin (TTP), significantly reduced or protected mice from inflammation, according to researchers at the National Institutes of Health. The results suggest that pharmaceutical compounds or other therapeutic methods that produce elevated levels of TTP in humans may offer an effective treatment for some inflammatory diseases, such as rheumatoid arthritis, psoriasis, and multiple sclerosis. The report appeared online Feb. 1 in the Proceedings of the National Academy of Sciences.

Eating healthier fats could reduce heart disease deaths worldwide

I bet your hospital has not had their nutritionist create diet protocols for stroke in and out of the hospital based upon the latest research. Ask when the diet protocol was last updated.
Do NOT do anything about this on your own, you know how dangerous eating is without your doctors prescription.
Even this seems to not account for the latest news on saturated fats, and it is from the American Heart Association. When you can't trust the American Heart Association to know what they are talking about you've lost the medical world as a professional source of information.

For decades, the government steered millions away from whole milk. Was that wrong?

Trans fats, not saturated fats, linked to increased mortality, CHD risks

Saturated Fat and CAD: It's Complicated
 

An Interview With The Big Fat Surprise Author Nina Teicholz

Nutrition Advice: Can We Stop the 'Low-Fat, Low-Carb' Lingo?

No Evidence to Support Dietary Fat Recommendations, Meta-Analysis Finds

Dairy Saturated Fats Lower Type 2 Diabetes Risk

CV Risk and Saturated Fats: The Debate Roils On

Dietary Saturated Fat Has Undeserved Bad Reputation, Says Review

New study puts final nail in the "saturated fat causes heart ...

Study Questions Fat and Heart Disease Link - NYTimes.com

Saturated Fats: Bad, Not Bad? - WebMD


Coconut oil: When saturated fat may be good for you

Olive Oil vs. Coconut Oil: Which is Heart-healthier ...

 

 

 


http://www.mdlinx.com/internal-medicine/top-medical-news/article/2016/02/10/1
Eating healthier fats could save more than a million people internationally from dying from heart disease, and the types of diet changes needed differ greatly between countries, according to new research in Journal of the American Heart Association. Eating healthier fats could save more than a million people worldwide from dying from heart disease each year. Refined carbohydrates and saturated fats should be replaced with heart–protective vegetable oils. While estimated deaths related to consumption of trans fats is on the decline in high–income countries, it is a growing problem worldwide because of the use of inexpensive partially–hydrogenated cooking fats in lower–income countries. To estimate the number of annual deaths related to various patterns of fat consumption, researchers used diet and food availability information from 186 countries, and research from previous longitudinal studies– which study people over long periods of time – on how eating specific fats influences heart disease risk. Using 2010 data, they estimate worldwide:
  • 711,800 heart disease deaths worldwide were estimated to be due to eating too little healthy omega–6 polyunsaturated fats, such as healthy vegetable oils, as a replacement for both saturated fats and refined carbohydrates. That accounted for 10.3 percent of total global heart disease deaths. In comparison, only about 1/3 of this – 250,900 heart disease deaths – resulted from excess consumption of saturated fats instead of healthier vegetable oils; accounting for 3.6 percent of global heart disease deaths. Saturated fats are found in meat, cheeses and –fat dairy products, as well as palm and coconut oils. The authors suggest that the difference is due to the additional benefits of increasing omega–6 polyunsaturated fats as a replacement for carbohydrates.
  • In addition, 537,200 deaths, which represent 7.7 percent of global heart disease deaths – resulted from excess consumption of trans fats, such as those in processed, baked, and fried goods as well as cooking fats used in certain countries.
Comparing 1990 to 2010, the investigators found that the proportion of heart disease deaths due to insufficient omega–6 polyunsaturated fat declined 9 percent and that due to high saturated fats declined by 21 percent. In contrast, deaths due to high consumption of trans fats rose 4 percent.

Health goes downhill when older adults stop driving

My doctor told me nothing about when or how I could get back to driving. Didn't even tell me anything about whether he had to report my driver license to the state as a result of my stroke. He was completely worthless. 2 years later I went on my own to another facility that had driver training,  The problem with that is that you get no practice time, you show up and are put in a car with a spinner knob and are expected to immediately function perfectly.
Is your doctor letting your health slide downhill because s/he has no stroke protocol on how to get back to driving?
http://www.mdlinx.com/internal-medicine/top-medical-news/article/2016/02/11/3
Study shows seniors experience double the risk of depressive symptoms, along with declines in cognition and physical functioning.
Researchers at Columbia University’s Mailman School of Public Health examined the health and well–being of older adults after they stopped driving and found that their health worsened in a variety of ways. In particular, driving cessation nearly doubled the risk of depressive symptoms, while also contributing to diminished cognitive abilities and physical functioning. Findings are published online in the Journal of the American Geriatrics Society. “For many older adults, driving is more than a privilege; it is instrumental to their daily living and is a strong indicator of self–control, personal freedom, and independence,” said Guohua Li, MD, DrPH, Mailman School professor of Epidemiology, the founding director of the Center for Injury Epidemiology and Prevention at Columbia, and senior author. “Unfortunately, it is almost inevitable to face the decision to stop driving during the process of aging as cognitive and physical functions continue to decline.”

Saturday, February 13, 2016

Scientific Literacy Redefined - Researchers could become better at engaging in public discourse by more fully considering the social and cultural contexts of their work

What we need most of all is how the research they do answers the questions/problems in stroke and where they are going next with their research. Since we have NO stroke leadership or strategy every single stroke researcher is on their own flailing in the dark.
http://www.the-scientist.com/?articles.view/articleNo/45102/title/Scientific-Literacy-Redefined/
Researchers could become better at engaging in public discourse by more fully considering the social and cultural contexts of their work.

Sensitive and effective conversations at end-of-life care after acute stroke

 From the Stroke Association- UK
http://www.strokeadvancingmodules.org/node.asp?id=palliative&

Senate recommends bill for improved NIH rehabilitation research

I don't know why they just didn't wholesale copy the National Alzheimer's Plan replacing Alzheimers with stroke.
http://www.healio.com/pediatrics/practice-management/news/online/%7B75fc3ccc-43e8-4738-836d-d21342585a79%7D/senate-recommends-bill-for-improved-nih-rehabilitation-research
The U.S. Senate Health, Education Labor and Pensions Committee recently voted to pass legislation to improve, coordinate and enhance medical rehabilitation research at the NIH.

The “Enhancing the Stature and Visibility of Medical Rehabilitation Research at the NIH Act” (S. 800), sponsored by Sens. Mark Kirk, R-Ill.; Michael Bennet, D-Colo.; Orrin Hatch, R-Utah; Lisa Murkowski, R-Alaska; Johnny Isakson, R-Ga.; and Susan Collins, R-Maine, calls for the development of a comprehensive research plan at the agency to conduct, support and coordinate research for the recovery of stroke victims and to help patients return to work. The bill also will establish a standard of care, opening access to specialized and intense care for patients struggling to recover from debilitating disabilities.

“The NIH strategic plan — which addresses the most complex war-time injuries, stroke, traumatic brain injuries and others — has not been updated since 1993,” Bennet said during the hearing. “This bill will set up benchmarks that the NIH has to meet and elevate rehabilitation research to senior-level expertise at the agency.”
Kirk, a stroke survivor, called for a higher standard of care for other Americans who have had strokes.
“After my stroke, intense rehabilitation at the Rehabilitation Institute of Chicago helped me get back on my feet and back to work,” Kirk said in a press release. “Every American should have the same access to quality rehab and care that I did. I thank my colleagues on the [Health, Education, Labor and Pensions (HELP)] Committee and look forward to passing this bill on the Senate floor.”
According to Bennet, the bill has been endorsed by leading members of the disability research community, including the March of Dimes, the National Multiple Sclerosis Society, the Paralyzed Veterans of America and the American Heart Association.
“Research into medical rehabilitation can help find new ways to improve recovery from stroke — a leading cause of serious, long-term disability,” Mark A. Creager, MD, president of the American Heart Association and director of the Heart and Vascular Center at Dartmouth-Hitchcock Medical Center, said in a press release. “The association stands in support of this important legislation, which will provide hope for those stroke survivors who need therapy to walk, talk and live independently again. We commend Sens. Kirk and Bennet and the HELP Committee for advancing it.”

According to Kirk, 75% of the 700,000 Americans who have a stroke each year will not return to work. Kirk said this bill will help those who are affected by stroke or other traumatic injuries to return to work and return to life as productive, healthy citizens.
“Coordination at the NIH is long overdue, and this legislation is a milestone for rehabilitation research,” Joanne C. Smith, MD, president and CEO of the Rehabilitation Institute of Chicago, said in a press release. “Its focus is aligned with [our] mission, ensuring continued best-in-class, scientifically driven care that advances patients’ ability and function.”

Scientists take a step closer to ETERNAL LIFE as they PRESERVE and REVIVE brain - rabbit

And with a hell of a lot of research we might be able to get our doctors to use this to stop the stroke progression and revive us when they have the ability to fix stroke sequela. Lots more to work out yet since the brain seems to have been removed from the head.
http://www.express.co.uk/news/science/643538/Scientists-take-a-step-closer-to-ETERNAL-LIFE-as-they-PRESERVE-and-REVIVE-brain

FOR the first time, scientists have successfully managed to cryogenically freeze a brain and then revive it.

In a step towards eternal life, researchers from 21st Century Medicine (21CM) managed to freeze the brain of a rabbit using a technique known as Aldehyde-stabilized cryopreservation (ASC).
The team, led by recent Massachusetts Institute of Technology graduate Robert McIntyre, wrote in a press release: "Using a combination of ultrafast chemical fixation and cryogenic storage, it is the first demonstration that near  perfect, long-term structural preservation of an intact mammalian brain is achievable.”

More at link.

 

Mapping neuroplastic potential in brain-damaged patients

 So maybe from this your doctor can tell how much neuroplasticity you can accomplish.

Mapping neuroplastic potential in brain-damaged patients

, , , ,
DOI: http://dx.doi.org/10.1093/brain/awv394 awv394 First published online: 8 February 2016


Summary

It is increasingly acknowledged that the brain is highly plastic. However, the anatomic factors governing the potential for neuroplasticity have hardly been investigated. To bridge this knowledge gap, we generated a probabilistic atlas of functional plasticity derived from both anatomic magnetic resonance imaging results and intraoperative mapping data on 231 patients having undergone surgery for diffuse, low-grade glioma. The atlas includes detailed level of confidence information and is supplemented with a series of comprehensive, connectivity-based cluster analyses. Our results show that cortical plasticity is generally high in the cortex (except in primary unimodal areas and in a small set of neural hubs) and rather low in connective tracts (especially associative and projection tracts). The atlas sheds new light on the topological organization of critical neural systems and may also be useful in predicting the likelihood of recovery (as a function of lesion topology) in various neuropathological conditions—a crucial factor in improving the care of brain-damaged patients.

Andago walks away with an IF Design Award - walking frame

Might be great for rehab centers, can't see any possibility for outpatient use. Research should be able to determine the efficacy of graduating from this to unsupported walking, but that won't occur. My partial body weight supported walking did not work because I needed full weight on my legs in order to  counteract the spasticity.
https://www.linkedin.com/pulse/andago-walks-away-design-award-mike-fuhrmann?trk=pulse_spock-articles













The video on the site misses the fact that this frame doesn't have a coffee holder.

This is really a good start into 2016.
IF International Forum Design GmbH is one of the oldest truly independent design institutions in the world and has been around since 1953 to identify, support and promote good design, to raise awareness of design among the public and to effect social change through design. This is the mission of the annual design competition, IF Design Award.
Frankly, I am really thrilled we won this award for our latest innovation Andago. An award like this is a wonderful opportunity to announce that Andago is now on its way to training floors in modern rehabilitation centers around the world. It’s amazing how many requests we are receiving since we presented our prototype on a handful selected events in 2015.
It also shows how much innovation power Hocoma has built up over the last years to really develop new disruptive robotic devices that have the power to shape and redefine modern and effective rehabiliation in future.
Worldwide, US-based MossRehab was the first rehabilitation facility to pilot therapy with the Andago.

“It’s guided by your own walking,” said Alberto Esquenazi, MD, MossRehab's chief medical officer explains. “The Andago will enable patients who’ve had a stroke or a traumatic brain injury to move more quickly from supported or assisted gait to unsupported walking".
A great opportunity to experience Adago will be the 9th World Congress for Neurorehabilitation (WCNR) that takes place in Philadelphia from May 10th to 13th, 2016.
We also just opened our registrations for a guided visit to MossRehab, Philadelphia’s largest provider of physical medicine and rehabilitation, on May 11th, 2016, to see and experience first-hand their state-of-the-art rehabilitation therapy. 
This special visit also includes lectures by some of the greatest experts in the field: MossRehab’s own Chief Medical Officer, Dr. Albert Esquenazi, and Prof. Dr. Leopold Saltuari, Head of Department of Neurology in Hochzirl, Austria, on the topic of Efficient Integration of New Technology into Clinical Practice in Rehabilitation.
So, grab your chance now to feel innovation first-hand as seats are limited.
Let's shape a better rehabilitation world in future.

15 Diseases and Ailments Marijuana May Help Fight

Because popular news articles like this do not contain uses for stroke stroke will never be added to medical marijuana laws. We need full legalization.
My 13 reasons for marijuana use post-stroke. Don't follow me but I will figure out some way to get some after my next stroke.

 Treating brain diseases with marijuana 

15 Diseases and Ailments Marijuana May Help Fight


1. & 2. Dravet syndrome and Lennox-Gastaut syndrome
3. Tuberous Sclerosis Complex (TSC)

4. Spasticity associated with multiple sclerosis
GW Pharmaceuticals also has Sativex, an approved oromucosal spray in 15 countries outside the U.S. that contains CBD and tetrahydrocannabinol, or THC, the hallucinogenic property of marijuana. In clinical studies Sativex was shown to reduce spasticity, or the tightness of muscles, in patients with multiple sclerosis.
5. Type 2 diabetes
6. Chemotherapy-induced nausea and vomiting & 7. Anorexia for patients suffering weight loss with AIDS
8. Chronic pain

9. Organ transplant rejection

10. Alzheimer's disease
Another potential benefit? How about treating Alzheimer's patients, of which there are about 5 million today, per the Alzheimer's Association. An abstract report published in the Journal of Alzheimer's Disease showed that at the six-hour, 24-hour, and 48-hour time marks THC lowered beta-amyloid levels in a dose-dependent manner. Beta-amyloid plaques are what stick to the brains of Alzheimer's patients, resulting in progressive cognitive decline.
11. Brain cancer
12. Schizophrenia

13. Parasitic infections

14. Glaucoma

15. Inflammatory bowel diseases



Dietary Nitrate Lowers Blood Pressure: Epidemiological, Pre-clinical Experimental and Clinical Trial Evidence

My last visit with my doctor had me asking about a nitric oxide diet. She said her clinic did not have one, diabetes, weight, gluten free were there. This abstract tells you nothing so ask your doctor for such a diet. I use beets but have no idea how much I should be eating on a daily basis.
http://www.ncbi.nlm.nih.gov/pubmed/26815004

Abstract

Nitric oxide (NO), a potent vasodilator critical in maintaining vascular homeostasis, can reduce blood pressure in vivo. Loss of constitutive NO generation, for example as a result of endothelial dysfunction, occurs in many pathological conditions, including hypertension, and contributes to disease pathology. Attempts to therapeutically deliver NO via organic nitrates (e.g. glyceryl trinitrate, GTN) to reduce blood pressure in hypertensives have been largely unsuccessful. However, in recent years inorganic (or 'dietary') nitrate has been identified as a potential solution for NO delivery through its sequential chemical reduction via the enterosalivary circuit. With dietary nitrate found in abundance in vegetables this review discusses epidemiological, pre-clinical and clinical data supporting the idea that dietary nitrate could represent a cheap and effective dietary intervention capable of reducing blood pressure and thereby improving cardiovascular health.

Friday, February 12, 2016

Choice of Human–Computer Interaction Mode in Stroke Rehabilitation - Fruit Ninja

The result of this should be a stroke protocol of how many hours of playing Fruit Ninja produces these results. But you and your doctor will need to guess because we have NO stroke leadership enforcing what should be produced from research.
http://nnr.sagepub.com/content/30/3/258?etoc
  1. Hossein Mousavi Hondori, PhD1
  2. Maryam Khademi, MEng1
  3. Lucy Dodakian, MA1
  4. Alison McKenzie, PhD2
  5. Cristina V. Lopes, PhD1
  6. Steven C. Cramer, MD1
  1. 1University of California, Irvine, CA, USA
  2. 2Chapman University, Orange, CA, USA
  1. Steven C. Cramer, MD, UC Irvine Medical Center, 200 S Manchester Ave, Suite 206, Orange, CA 92868-4280, USA. Email: scramer@uci.edu

Abstract

Background and Objective. Advances in technology are providing new forms of human–computer interaction. The current study examined one form of human–computer interaction, augmented reality (AR), whereby subjects train in the real-world workspace with virtual objects projected by the computer. Motor performances were compared with those obtained while subjects used a traditional human–computer interaction, that is, a personal computer (PC) with a mouse. 
Methods. Patients used goal-directed arm movements to play AR and PC versions of the Fruit Ninja video game. The 2 versions required the same arm movements to control the game but had different cognitive demands. With AR, the game was projected onto the desktop, where subjects viewed the game plus their arm movements simultaneously, in the same visual coordinate space. In the PC version, subjects used the same arm movements but viewed the game by looking up at a computer monitor.  
Results. Among 18 patients with chronic hemiparesis after stroke, the AR game was associated with 21% higher game scores (P = .0001), 19% faster reaching times (P = .0001), and 15% less movement variability (P = .0068), as compared to the PC game. Correlations between game score and arm motor status were stronger with the AR version.  
Conclusions. Motor performances during the AR game were superior to those during the PC game. This result is due in part to the greater cognitive demands imposed by the PC game, a feature problematic for some patients but clinically useful for others. Mode of human–computer interface influences rehabilitation therapy demands and can be individualized for patients.

Exploring the Evolution of Cortical Excitability Following Acute Stroke

The objective of this type of research should be defined protocols that promote functional recovery. But since we have NO leadership and NO strategy that objective in research is not going to occur.
http://nnr.sagepub.com/content/30/3/244?etoc
  1. William Huynh, PhD1,2
  2. Steve Vucic, PhD3
  3. Arun V. Krishnan, PhD2
  4. Cindy S-Y. Lin, PhD4
  5. Matthew C. Kiernan, DSc1
  1. 1Brain and Mind Research Institute, University of Sydney, New South Wales, Australia
  2. 2Prince of Wales Clinical School, University of New South Wales, New South Wales, Australia
  3. 3Western Clinical School, University of Sydney, New South Wales, Australia
  4. 4University of New South Wales, New South Wales, Australia
  1. William Huynh, PhD, Institute of Neurological Sciences, Prince of Wales Hospital, NSW 2031, Australia. Email: w.huynh@neura.edu.au

Abstract

Background. Evolution of changes in intracortical excitability following stroke, particularly in the contralesional hemisphere, is being increasingly recognized in relation to maximizing the potential for functional recovery. 
Objective. The present study utilized a prospective longitudinal design over a 12-month period from stroke onset, to investigate the evolution of intracortical excitability involving both motor cortices and their relationship to recovery, and whether such changes were influenced by baseline stroke characteristics.  
Methods. Thirty-one patients with acute unilateral ischemic stroke were recruited from a tertiary hospital stroke unit. Comprehensive clinical assessments and cortical excitability were undertaken at stroke onset using a novel threshold-tracking paired-pulse transcranial magnetic stimulation technique, and repeated at 3-, 6-, and 12-month follow-up in 17 patients who completed the longitudinal assessment.  
Results. Shortly following stroke, short-interval intracortical inhibition (SICI) was significantly reduced in both lesioned and contralesional hemispheres that correlated with degree of recovery over the subsequent 3 months. Over the follow-up period, ipsilesional SICI remained reduced in all patient groups, while SICI over the contralesional hemisphere remained reduced only in the groups with cortical stroke or more baseline functional impairment. 
Conclusions. The current study has demonstrated that evolution of intracortical excitability, particularly over the contralesional hemisphere, may vary between patients with differing baseline stroke and clinical characteristics, suggesting that ongoing contralesional network recruitment may be necessary for those patients who have significant disruptions to the integrity of ipsilesional motor pathways. Results from the present series have implications for the development of neuromodulatory brain stimulation protocols to harness and thereby facilitate stroke recovery.(What the hell is this?)

Faster Reaching in Chronic Spastic Stroke Patients Comes at the Expense of Arm-Trunk Coordination

Precisely how is this knowledge going to change your stroke protocols to recover better? No answer, then what the fuck use is this research?
http://nnr.sagepub.com/content/30/3/209?etoc
  1. Laurence Mandon, MD1,2
  2. Julien Boudarham, PhD2
  3. Johanna Robertson, PhD1,2
  4. Djamel Bensmail, MD PhD1,2
  5. Nicolas Roche, MD, PhD1,2
  6. Agnès Roby-Brami, MD, PhD2,3,4,5
  1. 1Raymond Poincaré Hospital, Garches, France
  2. 2GRCTH, EA4497, CIC-IT 805, CHU Raymond Poincaré, UVSQ, Garches, France
  3. 3CNRS, UMR 7222, ISIR, Paris, France
  4. 4Sorbonne Universités, UPMC University Pierre et Marie Curie, UMR 7222, Paris, France
  5. 5INSERM, U1150, Agathe-ISIR, Paris, France
  1. Agnès Roby-Brami, MD, PhD, UPMC University Pierre et Marie Curie, 4 place Jussieu, Paris, 75005, France. Email: roby-brami@isir.upmc.fr

Abstract

Background. The velocity of reaching movements is often reduced in patients with stroke-related hemiparesis; however, they are able to voluntarily increase paretic hand velocity. Previous studies have proposed that faster speed improves movement quality.  
Objective. To investigate the combined effects of reaching distance and speed instruction on trunk and paretic upper-limb coordination. The hypothesis was that increased speed would reduce elbow extension and increase compensatory trunk movement.  
Methods. A single session study in which reaching kinematics were recorded in a group of 14 patients with spastic hemiparesis. A 3-dimensional motion analysis system was used to track the trajectories of 5 reflective markers fixed on the finger, wrist, elbow, acromion, and sternum. The reaching movements were performed to 2 targets at 60% and 90% arm length, respectively, at preferred and maximum velocity. The experiment was repeated with the trunk restrained by a strap. Results. All the patients were able to voluntarily increase reaching velocity. In the trunk free, faster speed condition, elbow extension velocity increased but elbow extension amplitude decreased and trunk movement increased. In the trunk restraint condition, elbow extension amplitude did not decrease with faster speed. Seven patients scaled elbow extension and elbow extension velocity as a function of reach distance, the other 7 mainly increased trunk compensation with increased task constraints. There were no clear clinical characteristics that could explain this difference. Conclusions. Faster speed may encourage some patients to use compensation. Individual indications for therapy could be based on a quantitative analysis of reaching coordination.

Unexpected Expenses - Things to consider as you’re working on stroke recovery

Let's go back to cause and effect. The cause of inability to pay for these expenses is the losing of income due to disability from your stroke. You lessen than disability greatly if you stop the neuronal cascade of death. Solve the real problems, not just the aftereffects.  I really think that no one in positions of power and leadership in stroke has a brain at all. Send them to find the Wizard of Oz.
http://strokeconnection.strokeassociation.org/Winter-2016/Unexpected-Expenses/
Stroke in young adults can bring on money troubles that may be as challenging as the recovery itself.
“All patients, regardless of their insurance type, can have large medical expenses they are required to pay after their insurance has paid its portion,” said Erin Singleton, chief of mission delivery at the Patient Advocate Foundation (PAF). “Unlike other forms of debt, medical debt arises unexpectedly and is compounded by a decrease in income resulting from missed work either by themselves or those who act as a caregiver.”
With guidance, good choices for weathering stroke’s impact on your budget are possible. Here are some examples an
d guidance from others who’ve been there.

High-cholesterol diet, eating eggs do not increase risk of heart attack, not even in persons genetically predisposed

You can see if your doctor ever tells you that dietary cholesterol is not a problem. How long it takes before that occurs will tell you if your doctor follows any research at all. I expect my doctor to know more than me and know it before I do.
http://medicalxpress.com/news/2016-02-high-cholesterol-diet-eggs-heart-persons.html
A new study from the University of Eastern Finland shows that a relatively high intake of dietary cholesterol, or eating one egg every day, are not associated with an elevated risk of incident coronary heart disease. Furthermore, no association was found among those with the APOE4 phenotype, which affects cholesterol metabolism and is common among the Finnish population. The findings were published in the American Journal of Clinical Nutrition.
In the majority of population, dietary cholesterol affects serum cholesterol levels only a little, and few studies have linked the intake of dietary cholesterol to an elevated risk of cardiovascular diseases. Globally, many nutrition recommendations no longer set limitations to the intake of dietary cholesterol. However, in carriers of the apolipoprotein E type 4 allele - which significantly impacts cholesterol metabolism - the effect of dietary cholesterol on serum cholesterol levels is greater. In Finland, the prevalence of the APOE4 allele, which is a hereditary variant, is exceptionally high and approximately one third of the population are carriers. Research data on the association between a high intake of dietary cholesterol and the risk of cardiovascular diseases in this population group hasn't been available until now.
The of 1,032 men aged between 42 and 60 years and with no baseline diagnosis of a cardiovascular disease were assessed at the onset the Kuopio Ischaemic Heart Disease Risk Factor Study, KIHD, in 1984-1989 at the University of Eastern Finland. During a follow-up of 21 years, 230 men had a myocardial infarction, and 32.5 per cent of the study participants were carriers of APOE4.
The study found that a high intake of dietary cholesterol was not associated with the risk of incident - not in the entire study population nor in those with the APOE4 phenotype. Moreover, the consumption of eggs, which are a significant source of dietary cholesterol, was not associated with the risk of incident coronary . The study did not establish a link between dietary cholesterol or eating eggs with thickening of the common carotid artery walls, either.
The findings suggest that a high-cholesterol diet or frequent consumption of eggs do not increase the risk of cardiovascular diseases even in persons who are genetically predisposed to a greater effect of dietary cholesterol on serum . In the highest control group, the study participants had an average daily intake of 520 mg and they consumed an average of one egg per day, which means that the findings cannot be generalised beyond these levels.
More information: Associations of egg and cholesterol intakes with carotid intima-media thickness and risk of incident coronary heart disease according to apolipoprotein E phenotype in men: The Kuopio Ischaemic Heart Disease Risk Factor Study. American Journal of Clinical Nutrition ajcn122317; First published online February 10, 2016. DOI: 10.3945/ajcn.115.122317

Journal reference: American Journal of Clinical Nutrition search and more info website
Provided by: University of Eastern Finland search and more info website

Thursday, February 11, 2016

Dementia Dropping, But Will the Trend Continue?

Since they really don't know why there is absolutely no way to keep it dropping.
http://www.medpagetoday.com/Neurology/Dementia/56128?
The incidence of dementia in the U.S. has fallen over the last 3 decades, but that shouldn't lull providers into a false sense of complacency, researchers said.
In an analysis of data from the Framingham Heart Study, dementia incidence fell about 20% per decade since 1977, driven by declines in vascular dementia -- not Alzheimer's disease, Sudha Seshadri, MD, of Boston University, and colleagues reported in the New England Journal of Medicine
The drop has paralleled improvements in cardiovascular health and risk factor control, even though some contributors to heart disease -- and, potentially, dementia -- such as diabetes and obesity have been on the rise, they said.
Also, the significant declines in dementia were seen only among those who had at least a high school education, they noted.
"Our study offers cautious hope that some cases of dementia might be preventable or at least delayed," they wrote. "However, it also emphasizes our incomplete understanding of the observed temporal trend and the need for further exploration of factors that contribute to this decline in order to better understand and possibly accelerate this beneficial trend."
Researchers contacted by MedPage Today agreed that the findings do imply some hope for prevention, but physicians need to remain vigilant about cardiovascular risk factor control. And incidence can still rise as the population ages, said Alan Lerner, MD, of of UH Case Medical Center, who wasn't involved in the study, but warned that the "fight against dementia is far from over."
"The risk is still palpable, the aging of the population is still real, so in the real world we're still looking for prevention, whether that's secondary prevention for people with established risk factors such as a genetic predisposition or Alzheimer's disease, as well as control of vascular risk factors," Lerner said. "We know what's good for the heart is good for the brain ... so control of cardiovascular risk factors and leading a [healthy lifestyle] are still very important."
"So although in the overall sense the declining incidence of dementia would imply decreased risk," he added, "that risk has not gone away, and we need to continue to be vigilant and work to prevent dementia."
The Framingham Heart Study started in 1948, and dementia has been monitored since 1975. The current analysis included 5,205 people age 60 and up. There were a total of 371 cases of dementia over the study period.
Seshadri and colleagues found that the incidence of dementia fell during four different time periods in the study:
  • Late 70s to early 80s: 3.6 per 100
  • Late 80s to early 90s: 2.8 per 100
  • Late 90s to early 2000s: 2.2 per 100
  • Late 2000s to early 2010s: 2.0 per 100
Compared with the first time period, dementia incidence fell by 22%, 38%, and 44% over the next three time periods, respectively, they reported.
The findings also suggest that morbidity has been compressed, researchers said, given that the average age of onset of dementia has been increasing steadily -- from 80 in the earliest period to 85 in the latest.
Yet the overall risk reduction was seen only among those who had at least a high school education, who had about a 23% decline in risk per decade (P<0.001). There was no lowering of risk for those who didn't have a high school diploma, the researchers said.
They cautioned, however, that the proportion of those who didn't have a high school education was low during the last two time periods, so it precluded a deeper investigation into the trends in incidence of dementia in this subgroup.
During the course of the study, rates of cardiovascular events fell, while use of antihypertensives to control cardiovascular risk factors rose -- suggesting that earlier diagnosis and more effective treatment of stroke and heart disease may have contributed to a lower incidence of dementia, particularly vascular dementia. This benefit was also more pronounced in the population that had at least a high school education, the researchers said.
Seshadri and colleagues noted that the decline in incidence of Alzheimer's wasn't significant -- although analyses of dementia subtypes were based on smaller numbers than those for overall dementia, they cautioned.
In an accompanying editorial, David Jones MD, PhD, of Harvard, and Jeremy Greene, MD, PhD, of Johns Hopkins, warned that the data, while they align with other recent research, still reflect only one population sample.
"Whether they are accepted as conclusive evidence of a broad-based reduction in dementia incidence will become clear only over time," they wrote.
Also, since trajectories of chronic disease incidence "reflect complex interactions of many causal factors, it will almost always be uncertain whether decreases will continue or reverse," they added, citing the cardiovascular disease example. While heart disease began to wane in the mid-1960s -- and has continued to do so -- the ongoing increases in obesity and diabetes could reverse that trend. These two trends could affect dementia outcomes as well, they said.
Jason Karlawish, MD, of the University of Pennsylvania, who wasn't involved in the study, noted that the findings suggest researchers may need to revise the methods used to estimate the overall prevalence of dementia.
"We can't assume a static incidence," he said. "The incidence of risk factors is changing as well. Our projections didn't live up to our expectations with cardiovascular disease."

When People Ask How My Life Changed After Surviving a Hemorrhagic Stroke

My version is this:

Why my stroke was the best thing to ever happen to me'.


How My Life Changed After Surviving a Hemorrhagic Stroke

Halo Neuroscience raises $9M Series A for neurostimulation for athletics, stroke rehab

I don't have enough smarts to tell if the research behind this is decent enough to suggest commercial use. So ask your doctor, Halo does point to some research on their website. Neuropriming seems to be a made up word for marketing purposes.
http://medcitynews.com/2016/02/365959/
Post a comment /
/ Feb 10, 2016 at 3:47 PM
halo neurostim product shotHalo Neuroscience has launched a set of headphones and companion app to improve fitness performance through brain stimulation called Halo Sport, becoming the latest company to leap into the neurostimulation market.
More specifically, the company refers to its technology as neuropriming. It uses pulses of energy to accelerate strength and learning new skills.
It also raised a $9 million Series A round led by Lux Capital, with participation from Andreessen Horowitz, Jazz Venture Partners, SoftTech Ventures and Xfund.
The company is interested in applying its brain stimulation technology in two areas –athletics and stroke rehabilitation.
For that reason it stands apart from other companies that have focused on areas like ADHD, concentration in general, and de-stressing. In the area of stroke rehabilitation it has partnered with University of San Francisco Medical School and Medical University of South Carolina, to help it validate this application.
On the athletics side, it partnered with the  United States Ski & Snowboard Association, Invictus Crossfit and Michael Johnson Performance — an athletic training organization. Three Major League Baseball teams are also using the device.
It highlighted some of the results partners achieved with its neuropriming device in a company statement
The Olympic ski jumping team used its technology with the goal of improving propulsion for jumps. It saw a 13% gain in propulsion force.
The U.S. Military also used the technology to accelerate sniper training, according to Halo’s website.
The size of the neurostimulation device market is expected to rise to $8.79 billion by 2020, according to a report by Grand View Research.

How to reduce waste in research? From Edinburgh to Vienna and Sarajevo

I've been harping on this for years. Quite simple, you have a common database of all previous research and a leader who follows the strategy outlined. But we have shit for brains in current stroke leadership. NO leadership, NO strategy, NO database.
And our boards of directors must be ok with this failure.
https://monanasser.wordpress.com/2015/12/03/how-to-reduce-waste-in-research-from-edinburgh-to-vienna-and-sarajevo/

Computerized rehab aids those suffering from brain injuries

Well shit now all they have to do is write up a stroke protocol on this and we might be able to help survivors. But since we have NO leadership and NO strategy nothing will be followed up on this to help survivors. You're fucking screwed for the next 50 years at least. Maybe your great great grandchildren will be able to use this.
http://medicalxpress.com/news/2016-02-computerized-rehab-aids-brain-injuries.html
For the first time, researchers have shown that computerized cognitive rehabilitation (a program to help brain-injured or otherwise cognitively impaired individuals to restore normal functioning) can improve attention and executive functioning in brain injury survivors including traumatic brain injury (TBI) and stroke.
The findings, which appear online in the Journal of Head Trauma Rehabilitation, may lead to improved treatment outcomes in patients with , especially for patients with limited mobility and means and those residing in rural areas.
Persistent cognitive problems are very common following brain injury, especially in executive functioning, attention and learning.
The research team conducted a systematic literature review of computerized treatment for attention and in adults who suffered a brain injury. Studies published before or during April 2015 were evaluated for quality and methodology as no previous reviews had been completed. They found eight of 11 studies reported significant gains in cognitive function following treatment in TBI patients, with the three remaining studies reporting trends toward significance. Similarly, 10 of 12 mixed population studies observed significant improvements on measures of attention and executive function, with the remaining two studies reporting positive trends. Five studies reported significant improvements subsequent to treatment for stroke patients.
"The results of this systematic review provide encouraging evidence that computerized cognitive rehabilitation can improve attention and executive functioning in brain injury survivors," explained corresponding author Yelena Bogdanova, PhD, assistant professor of psychiatry at Boston University School of Medicine and principal investigator at the VA Boston Healthcare System.
According to the researchers computerized treatment delivery can significantly reduce the wait time and cost of treatment, provide immediate access to treatment in any location, improve the quality of life of patients and reduce the burden of caregivers.
Bogdanova believes further studies are needed. "It is important to evaluate the efficacy of computerized cognitive training programs and to provide specific guidelines for computerized methods of rehabilitation in patients with brain injury, as it can reduce cost and increase accessibility of to traditionally underserved populations," she added.
Journal reference: Journal of Head Trauma Rehabilitation search and more info website


Metabotropic NMDA receptor signaling couples Src family kinases to pannexin-1 during excitotoxicity - hyperacute saving of neurons

Stopping one of the causes of neuronal death.
Video TV report on this here:
http://calgary.ctvnews.ca/video?clipId=806097&binId=1.1201914&playlistPageNum=1#_gus&_gucid=&_gup=twitter&_gsc=mRhfBfW

The research here:
http://www.nature.com/neuro/journal/vaop/ncurrent/full/nn.4236.html
Nature Neuroscience
doi:10.1038/nn.4236
Received
Accepted
Published online

Abstract

Overactivation of neuronal N-methyl-D-aspartate receptors (NMDARs) causes excitotoxicity and is necessary for neuronal death. In the classical view, these ligand-gated Ca2+-permeable ionotropic receptors require co-agonists and membrane depolarization for activation. We report that NMDARs signal during ligand binding without activation of their ion conduction pore. Pharmacological pore block with MK-801, physiological pore block with Mg2+ or a Ca2+-impermeable NMDAR variant prevented NMDAR currents, but did not block excitotoxic dendritic blebbing and secondary currents induced by exogenous NMDA. NMDARs, Src kinase and Panx1 form a signaling complex, and activation of Panx1 required phosphorylation at Y308. Disruption of this NMDAR-Src-Panx1 signaling complex in vitro or in vivo by administration of an interfering peptide either before or 2 h after ischemia or stroke was neuroprotective. Our observations provide insights into a new signaling modality of NMDARs that has broad-reaching implications for brain physiology and pathology.

At a glance

Figures

left
  1. NMDA-induced dendritic blebbing is differentially blocked by noncompetitive and competitive antagonists.
    Figure 1
  2. Disrupting NMDA ligand binding blocks the secondary current.
    Figure 2
  3. NMDA-induced ionic dysregulation occurs during pore block by physiological Mg2+.
    Figure 3
  4. NMDAR-Src-Panx1 colocalize in a metabotropic signaling complex.
    Figure 4
  5. Activation of NMDAR-Src-Panx1 signaling during excitotoxicity requires phosphorylation of Src and Panx1.
    Figure 5
  6. Disrupting metabotropic NMDAR signaling prevented Panx1-mediated Ca2+ dysregulation, MPT and neuronal death during in vitro ischemia.
    Figure 6
  7. Blocking the NMDAR metabotropic signalsome reduces lesion size and sensorimotor deficits induced by stroke in vivo.
    Figure 7
  8. Acute Block of Panx1 does not inhibit NMDAR currents.
    Supplementary Fig. 1
  9. Activation of Excitotoxic Panx1 currents requires both ligand binding sites of NMDARs.
    Supplementary Fig. 2
  10. Pre-blocked NMDARs signal metabotropically to Panx1 during excitotoxicity.
    Supplementary Fig. 3
  11. GluN1 N616R pore mutation renders NMDARs Ca2+-impermeable.
    Supplementary Fig. 4
  12. NMDAR activation induces Panx1 phosphorylation at tyrosine 308.
    Supplementary Fig. 5
  13. Src mediated phosphorylation of Panx1 is Ca2+-independent.
    Supplementary Fig. 6
  14. TAT-Panx308 is a specific inhibitor of Src-mediated activation of Panx1.
    Supplementary Fig. 7
  15. Panx1 opening in the plasma membrane induces mitochondrial dysfunction during ischemia.
    Supplementary Fig. 8
  16. TAT-Panx308 does not alter cerebral blood flow under physiological conditions.
    Supplementary Fig. 9
  17. Full length blots cropped for representative figures.
    Supplementary Fig. 10
right