Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Saturday, March 28, 2015

The unsolved problems of neuroscience

You'll have to ask your neurologist what unsolved problems s/he is working on. Is figuring out exactly how neuroplasticity works and is made repeatable upon command one of them? If not you have only your stroke association to blame for not elevating that to a critical problem.
http://www.cell.com/trends/cognitive-sciences/abstract/S1364-6613%2815%2900023-6?
California Institute of Technology, Pasadena, CA, USA

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Some problems in neuroscience are nearly solved. For others, solutions are decades away. The current pace of advances in methods forces us to take stock, to ask where we are going, and what we should research next

Friday, March 27, 2015

Rowing wheelchair

Powered by a rowing motion. This would seem to be the way to go for survivors, it would force use of the affected arm and get you to thousands of repetitions much faster. But don't worry your doctor and therapists will not change and try something new for at least 50 years. And if we had anything approaching innovation from our stroke associations we could put together this rowing one with this mountain trike one.
http://www.yankodesign.com/2010/08/30/stand-up-wheelchair/
This post is about a wheelchair project which allows the user to stand up easily. “The Leeding E.D.G.E” also features easy drive handles with different gearing options to promote accessibility and combat shoulder injury generally caused by traditional wheeling techniques. Designer Time Leeding proposes this wheelchair alleviates pressure sores and makes moves toward closing social boundaries which “inhibit the lives of the disabled day to day.”
It is a world that I do not pretend for a moment to understand, that being the world that a person that must be in a wheelchair lives in. I believe that each person lives a different life, and that each person deals differently with a situation that they might not find ideal, for example becoming confined to a wheelchair partway through life. Does allowing a person with no use of legs the ability to stand up temporarily work toward a better life for that person?
That question asked, this wheelchair seems to me to be quite the fabulous looking bit of engineering. “The Leeding E.D.G.E” features “dynamic drive” handles that work with a rowing sort of motion. More energy efficient and less strenuous than traditional techniques. The chair features geared hubs featuring 2:1 drive, 1:1 drive, neutral and revers gears, and of course, that excellent standing mode.

Read more at http://www.yankodesign.com/2010/08/30/stand-up-wheelchair
 

NA-1 stroke drug a victory for basic research, says UPEI team

So I wonder which of the 5 causes of neuronal cascade of death this drug is addressing? Without that knowledge we really are just throwing darts in the dark.
http://www.cbc.ca/news/canada/prince-edward-island/na-1-stroke-drug-a-victory-for-basic-research-says-upei-team-1.3011749
A new stroke drug, which takes a new approach to treatment, shows the value of basic research, says a group of researchers at the University of Prince Edward Island.
The NA-1 drug treatment for stroke could change the landscape for the development of new drugs, says UPEI researcher Andy Tasker. (Maggie Brown/CBC)
The researchers did some of the research that led to the creation of the new drug. NA-1 will be tested by paramedics at five hospitals across the country as part of phase three clinical trials. Some members of the UPEI team also maintain part ownership of NoNO Inc., the company that is working to develop the drug and paying for the trials.
In previous trials, there was evidence the drug reduced cell death in stroke victims with minimal side-effects. NA-1 has so far shown to be beneficial for all types of stroke, not just ones caused by blood clots. Other medications are designed to break down clots in the brain, while NA-1 acts as a neuroprotectant, which enhances the brain's ability to withstand stroke.
Andy Tasker, one of the researchers who worked on the early stages of the drug at UPEI, said the latest trial is a watershed moment.
"If NA-1 proves effective in this trial it will change the landscape for the development of neuroprotectant drugs and is a wonderful endorsement of the value of investigator-driven, basic research in universities," said Tasker.
Tasker said this phase three trial is also a proud moment for the team at UPEI.
"To know that the part we played was critical in the development of this drug, to demonstrate that fundamental research really can lead to tangible benefits that benefit people in the real world in real time, and also frankly to show that a small university way out in the edges of the country can actually contribute to something which has the enormous potential to be a major impact worldwide," he said.
The trial began March 16 in Toronto and will then expand to other cities across Canada.

Medicare pay-for-value goals

I think this needs to be done even faster. I would highly suggest that as soon as you enter the hospital you inform the staff that payment is contingent upon full recovery. Unless we start holding our stroke medical professionals feet to the fire will we ever get significant advances in stroke recovery. The existing status quo is a complete f*cking failure.

HHS Doubles Down on the Shift from Volume to Value

 This might be the only way we will ever get our doctors and hospitals to actually get better results than the current failures of tPA only working completely 12% of the time10% full recovery rate and no stroke rehabilitation protocols.
However there is tremendous pushback from the medical world.

The Time Is Now To Fix Medicare ACOs

Accountable Care Organizations

Why should they be exempt from truth in labeling laws? If I am paying for a service, stroke rehab for example. Why should the 90% of people who don't fully recover pay for useless services?

Stroke Center Achieves New “Elite Plus” National Award - Ben Taub Hospital - Houston, TX

This is not recognizing results, this is recognizing doing processes which is a bunch of crap.  Everyone involved here would be fired under my watch.
You only focus on guidelines when you can't promote your results. If they were any good at all they would tell you their 30 day death rates, tPA efficacy percentage and full recovery percentage. But YOU are going to have to call the hospital presidents and tell them that this is totally unacceptable. If you don't light a fire under our stroke hospitals your next stroke recovery will be as bad as your current one.
Guidelines here: You can see how this is nothing to be impressed about. This is all indirect action, not results.
http://www.heart.org/HEARTORG/HealthcareResearch/GetWithTheGuidelinesHFStrokeResus/GetWithTheGuidelinesStrokeHomePage/Get-With-The-Guidelines-Stroke-Overview_UCM_308021_Article.jsp
Big f*cking whoopee.
http://www.newswise.com/articles/stroke-center-achieves-new-elite-plus-national-award

Ben Taub Hospital is the recipient of the American Heart Association/American Stroke Association’s Get With The Guidelines®- Stroke Gold Plus-Target: Stroke Honor Roll Elite Plus Award. The newly created elite award means the hospital achieved high marks for response and care provided for acute ischemic strokes(not results), the most common stroke—87 percent of all cases—in America.
The recognition places Harris Heath System’s Ben Taub Hospital among an exclusive group in southeast Texas capable of offering specialized care for the most complex stroke patients. The nationally-recognized hospital already boasts an impressive résumé of multiple certifications and commendations for its comprehensive stroke service. Comprehensive stroke centers are the largest and best-equipped hospitals in a given geographical area.

“This once again exhibits our staff’s commitment to excellence in patient care. To achieve this award, Ben Taub Hospital demonstrated 24 consecutive months of superior performance in the care of stroke patients. There is no higher recognition,” says Dr. Robert Trenschel, executive vice president and administrator, Ben Taub Hospital. “Most importantly this signifies that patients coming to Ben Taub Hospital will receive the highest quality care possible in the treatment of stroke and continues to fortify our position as a community asset. “
Stroke center certifications are an increasingly important way to demonstrate a stroke center's expertise and leadership. In Texas, the level of certification determines where trauma and EMS services will transport patients for the most appropriate stroke care.
“Our stroke program is successful because of the hard work and dedication from the stroke team members,” says Naylon Bird, manager, Stroke Program, Ben Taub Hospital. “Our multi-disciplinary team strives to go above and beyond to improve processes and assure that our patients receive the highest standard of stroke care.”
To receive the American Heart Association/American Stroke Association’s Get With The Guidelines®-Stroke Gold Plus-Target: Stroke Honor Roll Elite Plus, Ben Taub achieved an 85 percent or higher adherence to all program indicators for two or more consecutive 12-month intervals and achieved 75 percent or higher compliance with at least five of eight Get With The Guidelines-Stroke quality measures. Additionally, the Elite Plus recognition means the hospital achieved a door-to-needle time of 60 minutes or less in 75 percent of cases and, in at least 50 percent of cases, achieved door-to-needle times of 45 minutes or less.
“With a stroke, time lost is brain lost, and this award demonstrates Ben Taub’s commitment to being one of the top hospitals in the country for providing aggressive, proven stroke care,” says Dr. Joseph Kass, chief of Neurology and medical director of Stroke Service, Ben Taub Hospital, and associate professor, Department of Neurology, Baylor College of Medicine. “We will continue to focus on providing care to quickly and efficiently treat stroke patients with evidence-based protocols.”
Ben Taub Hospital also has a Comprehensive Stroke Center Certification awarded by DNV Healthcare, Inc. The DNV Comprehensive Stroke Center Certification is for three years and encompasses the full spectrum of stroke care—diagnosis, treatment, rehabilitation and education—and establishes clear metrics to evaluate outcomes. The hospital also is a designated comprehensive stroke center by the Southeast Texas Regional Advisory Council (SETRAC), a council that coordinates stroke, as well as other services such as trauma, to ensure the most efficient and best care available.
 

Positive Affect and Markers of Inflammation: Discrete Positive Emotions Predict Lower Levels of Inflammatory Cytokines. - Awe

Did you have any experiences of awe in the hospital at all? Mine consisted of awe at the total lack of knowledge my doctor had on getting me to recovery. Taking you out to view mountains would be a good start.
http://psycnet.apa.org/?&fa=main.doiLanding&doi=10.1037/emo0000033
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Stellar, Jennifer E.; John-Henderson, Neha; Anderson, Craig L.; Gordon, Amie M.; McNeil, Galen D.; Keltner, Dacher
Emotion, Jan 19 , 2015, No Pagination Specified.
Negative emotions are reliably associated with poorer health (e.g., Kiecolt-Glaser, McGuire, Robles, & Glaser, 2002), but only recently has research begun to acknowledge the important role of positive emotions for our physical health (Fredrickson, 2003). We examine the link between dispositional positive affect and one potential biological pathway between positive emotions and health—proinflammatory cytokines, specifically levels of interleukin-6 (IL-6). We hypothesized that greater trait positive affect would be associated with lower levels of IL-6 in a healthy sample. We found support for this hypothesis across two studies. We also explored the relationship between discrete positive emotions and IL-6 levels, finding that awe, measured in two different ways, was the strongest predictor of lower levels of proinflammatory cytokines. These effects held when controlling for relevant personality and health variables. This work suggests a potential biological pathway between positive emotions and health through proinflammatory cytokines.

A more understandable writeup here:

Experiences Of Art, Nature And Spirituality May Help Prevent Disease, Study Finds

A University of California, Berkeley, study, published in the journal Emotion in January, suggests that the feeling of awe we may experience during encounters with art, nature and spirituality has an anti-inflammatory effect, protecting the body from chronic disease. 

Thursday, March 26, 2015

The intriguing relationship between the ABO blood group, cardiovascular disease, and cancer

Well having type O- didn't seem to lower my cardiovascular risk enough to prevent my stroke, maybe it will prevent cancer.
http://www.biomedcentral.com/1741-7015/13/7

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Open Access Highly Accessed Commentary

The intriguing relationship between the ABO blood group, cardiovascular disease, and cancer

Massimo Franchini1* and Giuseppe Lippi2

1 Department of Hematology and Transfusion Medicine, C. Poma Hospital, Strada Lago Pajolo 10, Mantova, 46100, Italy
2 Laboratory of Clinical Chemistry and Hematology, Academic Hospital of Parma, Via Gramsci 14, Parma, 43100, Italy
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BMC Medicine 2015, 13:7  doi:10.1186/s12916-014-0250-y
The electronic version of this article is the complete one and can be found online at: http://www.biomedcentral.com/1741-7015/13/7

Received:17 November 2014
Accepted:9 December 2014
Published:16 January 2015
© 2015 Franchini and Lippi; licensee BioMed Central.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

Abstract

Other than being present at the surface of red blood cells, the antigens of the ABO blood group system are efficiently expressed by a variety of human cells and tissues. Several studies recently described the involvement of the ABO blood group in the pathogenesis of many human disorders, including cardiovascular disease and cancer, so that its clinical significance extends now beyond the traditional boundaries of transfusion medicine. In a large cohort study recently published in BMC Medicine and including over 50,000 subjects, Etemadi and colleagues reported that nearly 6% of total deaths and as many as 9% of cardiovascular deaths could be attributed to having non-O blood groups, a condition that was also found to be associated with increased risk of gastric cancer. In this commentary, the clinical implications of ABO blood groups are critically discussed and a possible common pathogenic mechanism involving the von Willebrand factor is described.
Keywords:
ABO blood group; Cancer; Cardiovascular disease; Mortality; von Willebrand factor

Background

The antigens of the ABO blood group system (i.e., A, B, and H antigens), discovered more than one century ago [1], are complex carbohydrate molecules expressed on the extracellular surface of red blood cell membranes [2]. The A and B alleles encode slightly different glycosyltransferases that add N-acetylgalactosamine and D-galactose to a common precursor side chain, the H determinant, which is then converted into A- or B-antigens, respectively (Figure 1). The O alleles do not encode a functional enzyme, so that OO carriers lack these transferase enzymes and express the unaltered H structure, with a solitary terminal fucose moiety attached to the precursor oligosaccharide chain, which represents the phenotypic marker of the O blood group [3]. In addition to the expression on red blood cell surfaces, the ABO antigens are also present in a variety of human cells and tissues, including epithelium, sensory neurons, platelets, and vascular endothelium [4],[5]. Therefore, it is not surprising that the clinical significance of the ABO blood group extends now beyond the traditional boundaries of immunohematology and transfusion medicine, wherein this antigen system is seemingly involved in the pathophysiology of a wide range of human diseases, the most important being represented by cancers and infectious and cardiovascular disorders [6]-[9].
thumbnailFigure 1. The intriguing relationship between ABO blood group system, von Willebrand factor (VWF), cancer and cardiovascular disease.

Discussion

A number of studies conducted in the past 50 years have consistently described the existence of an association between ABO blood type and cardiovascular disease [10]-[12]. In particular, a recent systematic review and meta-analysis documented that having a non-O blood group carries an approximately two-fold increased risk of venous thrombosis [10]. A weaker but still significant association was found in another systematic review conducted by the same group of authors between non-O blood type and arterial thrombosis (odds ratio [OR] of 1.28 for myocardial infarction and 1.17 for ischemic stroke) [11]. In addition to the effect of the ABO blood group on low-density lipoprotein and total serum cholesterol levels [13], the leading underlying mechanism that has been put forward to explain this association involves the profound influence that the ABO blood group system exerts on hemostasis, particularly on the von Willebrand factor (VWF) and, consequently, on coagulation factor VIII (FVIII) plasma levels, which are both well recognized prothrombotic risk factors [14]. Indeed, it is now clearly acknowledged that individuals of non-O blood group status have plasma levels of both VWF and FVIII that are approximately 25% higher than O blood group subjects [15]. The molecular basis of this phenomenon has been precisely identified with the presence of ABH antigenic structures on circulating VWF, which modulate the activity of this multifunctional protein through different degrees of glycosylation [12].
Another interesting field that has been extensively studied over the past five decades is that of the association between ABO blood group types and cancer [8],[9]. The most consistent association has been found with pancreatic and gastric cancers [8]. For instance, in the Nurses’ Health Study and Health Professionals Follow-up Study, Wolpin et al. [16] found that participants with blood groups A, AB, or B were more likely to develop pancreatic cancer compared with those with blood group O (adjusted hazard ratio [HR]: 1.44; 95% CI: 1.14–1.82). The higher prevalence of blood group A in patients with gastric cancer formerly observed by several studies [9] has also been recently confirmed in a large prospective population-based study involving more than one million of Scandinavian blood donors followed for up to 35 years [17]. The strength of this association was similar to that previously reported (OR: 1.20; 95% CI: 1.02–1.42). Although the underlying mechanisms linking the ABO blood group system and cancer are still largely unknown, one plausible explanation involves the ABO blood group-driven regulation of circulating levels of several proinflammatory and adhesion molecules (i.e., soluble E-selectin, P-selectin, and intercellular adhesion molecule-1), which play a key role in the tumorigenesis process [9]. Moreover, the recent discovery that VWF is an important modulator of angiogenesis and apoptosis provides an alternative, particularly intriguing, hypothesis to unify the mechanisms by which non-O blood group influences the onset of cardiovascular and neoplastic diseases (Figure 1) [18]. A significant advance in this field has now been provided by the Golestan Cohort Study, recently published in BMC Medicine[19]. This large epidemiological trial analyzed the association between ABO blood groups and overall and cause-specific mortality in over 50,000 people recruited between 2004 and 2008. Notably, the authors found that non-O blood groups were associated with a significantly increased risk of total death (HR: 1.09; 95% CI: 1.01–1.17) and mortality for cardiovascular disease (HR: 1.15; 95% CI: 1.03–1.27). Although no significant association was found with ABO-related cancer mortality, an aspect that was investigated for the first time in this study, an increased risk of developing gastric cancers was still observed in individuals with blood groups A and B. This latter finding is particular intriguing, and is also in keeping with the results from another recent study conducted by our group, in which a negative association between B blood group and life expectancy in a large cohort (n = 28,129) of subjects was found [20]. Although the analysis was only limited to overall mortality in our study, this evidence may be attributable to the association between B blood type and some aging associated conditions, including neurological and neoplastic disorders. Although additional research is needed to corroborate these preliminary findings, the attractive data that have emerged from these studies raise a new and intriguing scenario linking the ABO blood group with cardiovascular disease and cancer (Figure 1).

Conclusions

Despite being studied for more than half a century, the complex interplay between the ABO blood group system and human health is far from being definitely elucidated. In particular, if the association between non-O blood type and cardiovascular disease mortality is confirmed by further trials like that recently published by Etemadi et al. [19], non-O blood group status may be included in cardiovascular risk scores to better estimate the individual thrombotic risk profile. Further experimental studies are also needed to unravel the molecular mechanisms linking ABO blood type, VWF, and cancer development. Intuitively appealing, ABO blood typing may hence become part of a multifaceted strategy for cancer risk assessment.
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From a more readable source:
Cardiovascular Perks
Alexander says that it does look as though blood type O is protective in the setting of cardiovascular disease. “There is no reason to think that particular molecules on red blood cells would have anything to do with cardiovascular disease, but those same molecules attach molecules to a protein that is important in blood clotting, called the Von Willebrand factor,” she says. People with type O blood have lower Von Willebrand factor levels. That’s good for the heart because ”it means your blood is a little less likely to clot. And more heart attacks and strokes are caused by blood clots, so anything that can have a part in reducing that risk is beneficial.”

Stroke Rounds: Amino Acid in High-Protein Foods May Lower Stoke Risk

How much information does your doctor need before a post-stroke diet protocol is created?
http://www.medpagetoday.com/Cardiology/Strokes/50674?xid=nl_mpt_cardiodaily_2015-03-26&
High dietary intake of the non-essential, sulfur-containing amino acid cysteine was linked to lower stroke risk in a study of women living in Sweden.
High-protein foods such as beef, poultry and eggs are major sources of cysteine in the diet. Eating a high-protein diet has been linked with lower blood pressure and stroke risk in some studies, and the new research may explain this association, researcher Susanna C. Larsson, PhD, of the Karolinska Institute in Stockholm, and colleagues wrote in the journal Stroke.
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Women whose diets included the highest levels of cysteine had a 21% lower risk of stroke compared with women whose diets included the least amount of the amino acid.
"Our results further suggest that dietary cysteine may account, at least in part, for our previous observed inverse associations of total protein and animal protein intake with risk of stroke," the researchers wrote.
Dietary Protein and Blood Pressure
The data connecting dietary protein with blood pressure remain confusing.
A meta-analysis of 40 studies, published in 2012, found higher protein consumption to be associated with significant decreases in systolic and diastolic blood pressure and in a study from Boston University School of Medicine, published in 2014, researchers reported similar findings.
That study included participants in the Framingham Offspring Study between the ages of 30 and 54. Eating a high protein diet that was also high in fiber was associated with a 59% reduction in hypertension risk.
Other studies suggest that eating a primarily vegetarian, lower-protein diet is associated with lower blood pressure, including a meta-analysis of seven controlled trials and 32 observational studies published in 2014.
The newly published research expands on a 2012 study by Larsson and colleagues which found higher dietary protein intake to be inversely associated with stroke risk in women with hypertension.
"In this study we evaluated the a priori hypothesis that cysteine intake is inversely associated with risk of stroke, and that cysteine may have contributed to our previous observed finding for dietary protein," they wrote.
Only Cysteine Inversely Associated with Stroke Risk
Using data from the Swedish Mammography Cohort, which is a population-based prospective cohort of 34,250 women, the researchers identified 1,751 stroke cases during 10.4 years of follow-up. Cysteine intake was assessed through food frequency questionnaires, and the women also provided information on BMI, smoking status and history, and other relevant lifestyle factors.
Compared to women in the lowest quartile of cysteine intake (<559 mg/d), those with the highest intake (>703 mg/d) tended to be older, had a higher BMIs and were less likely to be current smokers and more likely to have a history of hypertension or diabetes.
Cysteine intake was found to be significantly inversely associated with risk of total stroke after adjustment for other stroke factors and total protein intake.
Among the findings:
  • Comparing the highest and lowest quintile of cysteine intake, the multivariable relative risk of total stroke was 0.79 (95% CI 0.65-0.97; P=0.04 for trend).
  • The corresponding relative risk was 0.82 (95% CI 0.65-0.97; P for trend = 0.12) for cerebral infarction and 0.54 (95% CI 0.29-1.03; P=0.08 for trend) for intracerebral hemorrhage.
  • Dietary intake of other amino acids, including proline and arginine, showed no independent association with stroke risk.
Potential study limitations cited by the researchers included the fact that food frequency and lifestyle questionnaires were self administered. But they noted that given the prospective study design, measurement error in assessing amino acid intake would be unlikely to be related to outcomes.
They further noted that because the study was observational, it cannot prove cause and effect. Several previous studies examining the association between amino acid intake and stroke risk have failed to show a protective role for dietary cysteine with regard to blood pressure.
"We observed an inverse association between dietary cysteine intake and risk of stroke," the researchers concluded. "Our findings further suggest that cysteine, at least partly, may account for the reported inverse relation between animal protein intake and stroke risk. These results warrant confirmation by other prospective studies and randomized trials."

Lake Regional Hospital earns Level II Stroke Center designation - Osage Beach MO

I hate these backpatting displays. Nothing in here says the RESULTS were better.
Call the hospital president(Michael E. Henze - Chief Executive Officer) and demand better stroke results than this crap.


Big f*cking whoopee.
You can check out Joint Commission standards here:
 I saw absolutely nothing about what should be done the first week or anything about measuring 30-day deaths and 100% recovery.  God, these people are worse than worthless. Complacent good-for-nothings. 
http://www.lakenewsonline.com/article/20150324/NEWS/150329526/1994/NEWS
Time is crucial in stroke treatment. To help emergency medical care response teams provide the best care possible(What about results?) the shortest amount of time, the Missouri Department of Health and Senior Services has identified hospitals across the state that are equipped to provide definitive care to stroke patients. Lake Regional Health System is proud to announce it is one of these hospitals, earning the designation of Level II Stroke Center.
“As a Level II Stroke Center, Lake Regional offers comprehensive stroke care and recovery, including treatment from board-certified neurologists, specially trained Emergency Department physicians and staff, and rehabilitation services,” said Philip Kurle, M.D., a neurologist with Lake Regional Neurology in Osage Beach. “As a result, Lake Regional offers definitive stroke care for acute patients. In addition, rather than having to transfer stroke patients on to another hospital, Lake Regional can receive transfers from other care centers.”
Stroke Treatment at Lake Regional
According to the American Heart Association, someone in the U.S. has a stroke about once every 40 seconds. During a stroke, a blood vessel carrying oxygen and vital nutrients to the brain is either blocked by a clot or ruptures. As a result, part of the brain is deprived of blood and oxygen, destroying valuable nerve cells in the affected area within minutes.
The first hour after the onset of stroke symptoms is often referred to as the “golden hour.” That’s when the clot-buster drug tPA has shown the most benefit to restore blood flow and prevent further cognitive and physical problems. As a Level II Stroke Center, Lake Regional can administer this potentially lifesaving drug.
“If received in time, this drug can reduce the stroke’s permanent effects and make a full recovery more likely,” Dr. Kurle said.
When patients arrive at Lake Regional with a suspected stroke, the Emergency Department immediately calls in a neurologist. Patients receive rapid evaluation, on average seeing an ED physician or neurologist within five minutes of arriving. Next come an emergency CT scan and MRI, to determine whether the problem is insufficient blood flow (ischemic stroke), a ruptured blood vessel (hemorrhage) or some other condition.
In cases of ischemic stroke, the American Stroke Association guidelines call for patients to receive tPA within one hour of arriving at the hospital. Last year, Lake Regional did much better than this goal, averaging just 47 minutes from patient arrival to tPA administration.
“This rapid response is focused on limiting the effects of the stroke as much as possible,” Dr. Kurle said. “The next stage of treatment puts the focus on helping patients recover any losses.”
The Lake Regional nurses and rehab therapists have specialized training in stroke care. All therapy, including physical, occupational and speech therapy, begins on Day 1. Patients are assessed and receive therapies based on their needs.

Glutamate and GABA Imbalance Following Traumatic Brain Injury

You'll have to have your doctor get this and see if any of the therapeutic interventions can be repurposed for stroke.  I am assuming all along that your doctor is doing this on a weekly basis and is constantly coming up with new rehabilitation interventions all the time.
http://link.springer.com/article/10.1007/s11910-015-0545-1
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Abstract

Traumatic brain injury (TBI) leads to multiple short- and long-term changes in neuronal circuits that ultimately conclude with an imbalance of cortical excitation and inhibition. Changes in neurotransmitter concentrations, receptor populations, and specific cell survival are important contributing factors. Many of these changes occur gradually, which may explain the vulnerability of the brain to multiple mild impacts, alterations in neuroplasticity, and delays in the presentation of posttraumatic epilepsy. In this review, we provide an overview of normal glutamate and GABA homeostasis and describe acute, subacute, and chronic changes that follow injury. We conclude by highlighting opportunities for therapeutic interventions in this paradigm.



God is a good bartender - wine

Even God endorses wine. Although you will notice that God seems to prefer women. I guess us guys get the dregs.

Hospital for advanced rehab opens in capital - Amana Healthcare - Abu Dhabi

This is great but with no mention of actual proven results this is all just puffery. YOU will need to demand efficacy percentages or we will once again not know which therapy programs actually work. Your medical teams prefer this because then they get paid regardless of how well their interventions work. With only a 10% full recovery rate current rehab is a total failure. Are they any better than that 10%?
http://gulfnews.com/xpress/abu-dhabi/news/hospital-for-advanced-rehab-opens-in-capital-1.1478807

£1.1m study to reduce cognitive problems in people with MS

I can easily see being able to reuse this for stroke survivors. What is your doctor doing to follow this and create a cognitive stroke protocol for you? ANYTHING AT ALL?
http://www.alphagalileo.org/ViewItem.aspx?ItemId=151130&CultureCode=en
Experts in Nottingham are leading a major new study into how people with multiple sclerosis (MS) could overcome problems with attention and memory associated to their condition.
The Cognitive Rehabilitation for Attention and Memory in people with Multiple Sclerosis (CRAMMS) trial will evaluate the effectiveness of new strategies to improve and compensate for these difficulties and aims to improve the quality of life for the patient.
The trial is being led by Nadina Lincoln, Professor of Clinical Psychology in the Division of Rehabilitation and Ageing at The University of Nottingham and Dr Roshan das Nair, consultant clinical psychologist at Nottingham University Hospitals NHS Trust and honorary Associate Professor in the University’s Division of Rehabilitation and Ageing.
Funded by the National Institute for Health Research (NIHR) Health Technology Assessment (HTA) programme, the trial will begin recruiting participants later this month.
Professor Lincoln said: “The purpose of our research is to help people with multiple sclerosis boost their everyday memory so they can get on with their lives and do the things that people take for granted, for example remembering to pick their children up from school, turning the stove off, or knowing where they have put things.
“It will also provide them with strategies to enable them to concentrate on information without getting distracted.”
Memory and attention problems are common complaints for those who have multiple sclerosis. More than 100,000 people in the UK have multiple sclerosis and of these, 50,000 will have problems with attention and memory at some stage in the progression of their condition.
Very few people with multiple sclerosis get treatment for cognitive problems in usual clinical practice, despite some evidence that cognitive rehabilitation may help reduce problems in attention and everyday forgetting. However, cognitive rehabilitation for people with multiple sclerosis has not been demonstrated to be effective or cost-effective in large-scale randomised controlled trials.
The study will be exploring the benefits of using internal memory aids, such as mnemonics — using patterns, words and images to remember details — and external aids, such as diaries, mobile phones and cameras. The researchers will also be looking for other imaginative ways to help improve memory and reduce forgetting.
The study is being conducted in collaboration with Swansea University, Nottingham University Hospitals NHS Trust, Sheffield Teaching Hospitals NHS Trust, The Walton Centre NHS Trust, and University Hospitals Birmingham NHS Trust.
They will recruit 400 volunteers, aged 16 to 69 years, from NHS hospitals, rehabilitation centres, multiple sclerosis charities, and web forums. About half the volunteers will then receive a 10-week group intervention at one of the study centres in Nottingham, Sheffield, Liverpool and Birmingham. The groups will focus on strategies to improve attention and to reduce memory problems in daily life. The remaining volunteers will continue to receive their existing level of care.
If this study confirms the benefits of cognitive rehabilitation it could lead to a change in clinical practice in the NHS and abroad. The researchers will also use questionnaires to determine the cost-effectiveness of this intervention, and to get feedback from those taking part in the trial to establish if intervention improved their quality of life.
http://www.nottingham.ac.uk/news/pressreleases/2015/march/11m-study-to-reduce-cognitive-problems-in-people-with-ms.aspx

Nanorobotic agents open the blood-brain barrier, offering hope for new brain treatments

Now if we just had a strategy to identify candidate drugs for this. Ask your neurologist whom the hell needs to be contacted to identify drugs for this purpose. If your neurologist doesn't know that call the hospital president and have that person relieved of duty for not knowing how to practice medicine. If WE don't start taking a hard line with our stroke medical staff they will never fix any of the problems in stroke. Heads need to start rolling. Ranting in full force today, the president of the WSO really needs to justify the incompetency of that organization.
http://www.alphagalileo.org/ViewItem.aspx?ItemId=151118&CultureCode=en
Magnetic nanoparticles can open the blood-brain barrier and deliver molecules directly to the brain, say researchers from the University of Montreal, Polytechnique Montréal, and CHU Sainte-Justine. This barrier runs inside almost all vessels in the brain and protects it from elements circulating in the blood that may be toxic to the brain. The research is important as currently 98% of therapeutic molecules are also unable to cross the blood-brain barrier. “The barrier is temporary opened at a desired location for approximately 2 hours by a small elevation of the temperature generated by the nanoparticles when exposed to a radio-frequency field,” explained first author and co-inventor Seyed Nasrollah Tabatabaei. “Our tests revealed that this technique is not associated with any inflammation of the brain. This new result could lead to a breakthrough in the way nanoparticles are used in the treatment and diagnosis of brain diseases,” explained the co-investigator, Hélène Girouard. “At the present time, surgery is the only way to treat patients with brain disorders. Moreover, while surgeons are able to operate to remove certain kinds of tumors, some disorders are located in the brain stem, amongst nerves, making surgery impossible,” added collaborator and senior author Anne-Sophie Carret.
Although the technology was developed using murine models and has not yet been tested in humans, the researchers are confident that future research will enable its use in people. “Building on earlier findings and drawing on the global effort of an interdisciplinary team of researchers, this technology proposes a modern version of the vision described almost 40 years ago in the movie Fantastic Voyage, where a miniature submarine navigated in the vascular network to reach a specific region of the brain,” said principal investigator Sylvain Martel. In earlier research, Martel and his team had managed to manipulate the movement of nanoparticles through the body using the magnetic forces generated by magnetic resonance imaging (MRI) machines.
To open the blood-brain barrier, the magnetic nanoparticles are sent to the surface of the blood-brain barrier at a desired location in the brain. Although it was not the technique used in this study, the placement could be achieved by using the MRI technology described above. Then, the researchers generated a radio-frequency field. The nanoparticles reacted to the radio-frequency field by dissipating heat thereby creating a mechanical stress on the barrier. This allows a temporary and localized opening of the barrier for diffusion of therapeutics into the brain.
The technique is unique in many ways. “The result is quite significant since we showed in previous experiments that the same nanoparticles can also be used to navigate therapeutic agents in the vascular network using a clinical MRI scanner,” Martel remarked.  “Linking the navigation capability with these new results would allow therapeutics to be delivered directly to a specific site of the brain, potentially improving significantly the efficacy of the treatment while avoiding systemic circulation of toxic agents that affect healthy tissues and organs,” Carret added. “While other techniques have been developed for delivering drugs to the blood-brain barrier, they either open it too wide, exposing the brain to great risks, or they are not precise enough, leading to scattering of the drugs and possible unwanted side effect,” Martel said.
Although there are many hurdles to overcome before the technology can be used to treat humans, the research team is optimistic. “Although our current results are only proof of concept, we are on the way to achieving our goal of developing a local drug delivery mechanism that will be able to treat oncologic, psychiatric, neurological and neurodegenerative disorders, amongst others,” Carret concluded.

Power Vest - Orthosis helps avoid incorrect movements

This may be meant for health care workers but I could easily see it being useful for survivors. Ask your doctor what the hell they are doing about this for you.
http://www.alphagalileo.org/ViewItem.aspx?ItemId=151116&CultureCode=en
Each year millions of people within the EU injure themselves in the course of their work due to picking up heavy loads or from one-sided movements – ending up with serious health issues. Together with the industry, Fraunhofer researchers are developing a vest designed to take the burden off caregivers and others with physically demanding jobs.
In Germany, back pain is a national complaint, with nearly ten percent of all lost working days attributable to lower back problems, according to the 2014 Health Report published by the Techniker Krankenkasse. The study found that occupation had a significant impact on the duration and frequency of time taken off due to poor health. Caregivers are particularly affected, because working in a hospital or nursing home requires physical strength. There are patients to move, mobilize and help up – and all that puts the musculoskeletal system under stress. Now, modern technology offers caregivers’ backs extra support. In the “CareJack” project, researchers from the Fraunhofer Institute for Production Systems and Design Technology IPK and the Fraunhofer Institute for Reliability and Microintegration IZM, both in Berlin, are working together with industry partners to develop an active vest designed for these kinds of workers. Cleverly, this non-bulky orthosis (a short form of orthopedic prosthesis) is light, soft and comfortable to wear. That means it can be worn over regular clothes like a coat. Experts call it soft robotics.
“Until now, there haven’t been any efficient support systems to help caregivers with the heavy work they encounter in their extremely varied day-to-day work,” says IPK expert Henning Schmidt, who heads up the project. Anyone working in hospitals, nursing homes or outpatient care needs a strong back. But how can you provide the spine with support without limiting its abundant range of motion? Schmidt and his team have joined forces with company partners to strike out on a new path. Rather than relying on the hard shells often used in orthoses, they’ve instead opted for a material that is flexible and comfortable to wear. All the electronics are incorporated into the material.
The energy required comes from the wearers themselves, through their movements. When a caregiver bends down to lift a patient up, the smart medical aid stores the kinetic energy and can release it again when required.
Orthosis helps avoid incorrect movements
Above all, the orthosis ensures that caregivers perform movements correctly. Lots of orthopedic problems are a result of improper movements: the classic example is lifting something heavy with a rounded back instead of squatting down to lift the object with a straight back. The smart vest features a myriad of sensors that continuously monitor the way the wearer is moving. A processor compares these data against the optimum movement pattern. As soon as it detects any irregularity, a warning lamp is activated. Not only that, but innovative synthetic actuators with adjustable rigidity help avoid incorrect movements and support correct ones. “The wearer can decide themselves what level of support they want,” says Schmidt.
Functions of this sophistication call for a large amount of electronic equipment. “Still, nobody wants to haul around a backpack full of electronics,” says IZM expert Erik Jung. In the CareJack project, he and his team collaborated with company partners to develop miniaturized components, flexible circuit boards and all the necessary sensors. A prototype of the vest should appear in 2015, and Schmidt estimates it will be in series production in one to two years. The demand, he points out, is extremely high. It’s not just caregivers who could make use of this sort of active support, but anyone performing heavy physical work – construction workers, roofers, garbage collectors, brick layers and many more.
https://www.fraunhofer.de/en/press/research-news/2015/March/power-vest.html
The CareJack vest supports the back without restricting freedom of movement.
© Fraunhofer IPK/IZM

Head injury patients show signs of faster ageing in the brain

Inquiring minds want to know what this would say about stroke survivors. But it won't occur because our stroke associations are not innovative enough to even try to find answers to any stroke question.
So we are left with this very old statement. Compared with the normal rate of neuron loss in brain aging, the ischemic brain ages 3.6 years each hour without treatment.
http://www.alphagalileo.org/ViewItem.aspx?ItemId=151080&CultureCode=en
People who have suffered serious head injuries show changes in brain structure resembling those seen in older people, according to a new study.
Researchers at Imperial College London analysed brain scans from over 1,500 healthy people to develop a computer program that could predict a person's age from their brain scan. Then they used the program to estimate the "brain age" of 113 more healthy people and 99 patients who had suffered traumatic brain injuries.
The brain injury patients were estimated to be around five years older on average than their real age.
Head injuries are already known to increase the risk of age-related neurological conditions such as dementia later in life. The age prediction model may be useful as a screening tool to identify patients who are likely to develop problems and to target strategies that prevent or slow their decline.
"Your chronological age is not necessarily the best indicator of your health or how much longer you will live," said Dr James Cole, who led the study, from the Department of Medicine at Imperial College London. "There is a lot of interest in finding biomarkers of ageing that can be used to measure a certain aspect of your health and predict future problems."
The study, published in the April issue of Annals of Neurology, used magnetic resonance imaging (MRI) to study changes in brain structure. The researchers used a machine learning algorithm to develop a computer program that could recognise age-related differences in the volume of white matter and grey matter in different parts of the brain.
The model was then used to estimate subjects' ages based on their brain scans. The study included 99 patients with traumatic brain injuries (TBI) caused by road accidents, falls or assaults, who had persistent neurological problems. The scans were taken between one month and 46 years after their injuries.
In healthy controls, the average difference between predicted age and real age was zero. In TBI patients, the difference was significantly higher, with a bigger discrepancy in patients with more severe injuries. Bigger differences in predicted age were associated with cognitive impairments such as poor memory and slow reaction times.
There was also a correlation between time since injury and predicted age difference, suggesting that these changes in brain structure do not occur during the injury itself, but result from ongoing biological processes, potentially similar to those seen in normal ageing, that progress more quickly after an injury.
"Traumatic brain injury is not a static event," said Dr Cole. "It can set off secondary processes, possibly related to inflammation, that can cause more damage in the brain for years afterwards, and may contribute to the development of Alzheimer's or other forms of dementia."
The researchers believe the age prediction model could be applied not just to TBI patients, but might also be useful to screen outwardly healthy people.
"We want to do a study where we use the program to estimate brain age in healthy people, then see if the ones with 'old brains' are more likely to get neurodegenerative diseases. If it works, we could use it to identify people at high risk, enrol them in trials and potentially prescribe treatments that might stave off disease," said Dr Cole.
The researchers received funding from the EU Seventh Framework Programme and a National Institute for Health Research (NIHR) professorship for Professor David Sharp. The research was also supported by the NIHR Imperial Biomedical Research Centre.

Use of Stent Increases Risk of Stroke in Patients With Intracranial Arterial Stenosis

Be careful out there.
http://dgnews.docguide.com/use-stent-increases-risk-stroke-patients-intracranial-arterial-stenosis?overlay=2&
Among patients with symptomatic intracranial arterial stenosis, the use of a balloon-expandable stent compared with medical therapy resulted in an increased risk of stroke or transient ischemic attack (TIA), according to a study published in the March 24/31 issue of JAMA.
Intracranial arterial stenosis is a common cause of stroke worldwide. The recurrent stroke risk with severe symptomatic intracranial stenosis may be as high as 23% at 1 year, despite medical therapy, according to Osama O. Zaidat, MD, Medical College of Wisconsin/Froedtert Hospital, Milwaukee, Wisconsin, and colleagues.

But they don't explain whether the strokes were downstream or close to the stent or in a completely different area. Don't these people know how to analyze cause and effect? If someone has stenosis it is probably throughout the brain so a stroke would be likely regardless of fixing one particular spot.

Can Lithium Benefit Brain Health?

What does your doctor have to say about the neuroprotective and neurogenesis benefits? Is this proven enough to create a stroke protocol? References are at the bottom of the article.
http://www.life-enhancement.com/magazine/article/952-can-lithium-benefit-brain-health
A couple of intriguing paragraphs:

Lithium Protects Against Neuronal Death
In a third study, researchers examined the effects of lithium on glutamate-induced excitotoxicity, which is neuronal death caused by excessive amounts of glutamate, the brain’s most prevalent neurotransmitter.4 This phenomenon has been strongly implicated in the origin of a variety of neurodegenerative diseases, including dementia. The researchers found that lithium in the therapeutic range largely prevented glutamate-induced excitotoxicity in rodent cortical neurons. It apparently did so by stimulating the production of a protective protein called brain-derived neurotrophic factor, or BDNF, which is vital for the development and maintenance of healthy neurons (neurotrophic means pertaining to neural nutrition). Evidence for this mechanism came from the observation that when an antibody that neutralizes BDNF was added to the culture, lithium’s neuroprotective effect was blocked.
Lithium Stimulates New Neuronal Growth
Protecting neurons from destruction is one thing; it’s quite another to stimulate the growth of new neurons—a process called neurogenesis.* Numerous factors can affect neurogenesis, and lithium is apparently one of them. Researchers treated mice with lithium in dosages that produced plasma concentrations equivalent to those in the human therapeutic range; then they killed the mice and examined their brains.5 They found a 25% increase in the number of dividing cells in a structure of the hippocampus called the dentate gyrus—a clear indication of neurogenesis. This fit with the fact that lithium is known to stimulate production of a brain protein called B-cell lymphoma protein-2 (bcl-2) in certain areas of rodent brains; bcl-2 not only actively protects neurons from a variety of threats, including apoptosis (programmed cell suicide), but also promotes new cell growth. (Hippocampal neurogenesis has also been observed with a variety of antidepressants, so lithium’s action in this regard is not unique.)

Lithium Increases Gray Matter

MRI of human brain: actual (left) and artificially colored (right) to illustrate different neuroanatomical features.
Finally, researchers at the Wayne State University School of Medicine in Detroit studied ten human patients (average age 33) with bipolar disorder.6 For 4 weeks they gave the patients a daily therapeutic dosage of lithium (they didn’t specify the actual dosage, but rather the plasma lithium-ion concentration that resulted from it—about 0.8 millimoles per liter, which would have required roughly 1000 mg per day of lithium carbonate). They then did magnetic resonance imaging (MRI) of the patients’ brain and compared the scans with those taken at the outset of the study. In eight of the ten patients’ brains, the lithium treatment significantly increased the total volume of gray matter: the average increase was 3%, corresponding to a volume of about 24 cm3 (1.5 in.3). The authors attributed the effect to lithium’s neurotrophic properties and its ability to stimulate the growth of such non-neuronal objects as glial cells, but they did not describe it as neurogenesis. 


Will your doctor do ANYTHING AT ALL with this information? What about your stroke association or hospital? I'd be willing to bet that these lazy f*ckers will do nothing. The excuse will be that 'There are no clinically proven studies on this'. Shit, then run the goddammed studies yourself.

Entrepreneur’s app offers way for intoxication to be measured in the eyes - but what about survivors?

If we had a great stroke association we could ask them to follow up with this company to make sure that deficits from stroke don't automatically show up as you being drunk when you're not. But we do have craptastic ones that put out press releases. And the board of directors seems to be ok with that style of failure.
http://medcitynews.com/2015/03/entrepreneurs-app-offers-way-intoxication-measured-eyes/?

Wednesday, March 25, 2015

Carbon nanotube fibers make superior links to brain

And with this our researchers could listen in to signals between neurons and learn exactly what signals are sent between neurons to cause neuroplasticity to work.
http://www.rdmag.com/news/2015/03/carbon-nanotube-fibers-make-superior-links-brain?
Carbon nanotube fibers invented at Rice Univ. may provide the best way to communicate directly with the brain.
The fibers have proven superior to metal electrodes for deep brain stimulation and to read signals from a neuronal network. Because they provide a two-way connection, they show promise for treating patients with neurological disorders while monitoring the real-time response of neural circuits in areas that control movement, mood and bodily functions.
New experiments at Rice demonstrated the biocompatible fibers are ideal candidates for small, safe electrodes that interact with the brain’s neuronal system, according to the researchers. They could replace much larger electrodes currently used in devices for deep brain stimulation therapies in Parkinson’s disease patients.
They may also advance technologies to restore sensory or motor functions and brain-machine interfaces as well as deep brain stimulation therapies for other neurological disorders, including dystonia and depression, the researchers wrote.
The paper appeared online in ACS Nano.
The fibers created by the Rice lab of chemist and chemical engineer Matteo Pasquali consist of bundles of long nanotubes originally intended for aerospace applications where strength, weight and conductivity are paramount.
The individual nanotubes measure only a few nanometers across, but when millions are bundled in a process called wet spinning, they become thread-like fibers about a quarter the width of a human hair.
“We developed these fibers as high-strength, high-conductivity materials,” Pasquali said. “Yet, once we had them in our hand, we realized that they had an unexpected property: They are really soft, much like a thread of silk. Their unique combination of strength, conductivity and softness makes them ideal for interfacing with the electrical function of the human body.”
The simultaneous arrival in 2012 of Caleb Kemere, a Rice assistant professor who brought expertise in animal models of Parkinson’s disease, and lead author Flavia Vitale, a research scientist in Pasquali’s lab with degrees in chemical and biomedical engineering, prompted the investigation.
“The brain is basically the consistency of pudding and doesn’t interact well with stiff metal electrodes,” Kemere said. “The dream is to have electrodes with the same consistency, and that’s why we’re really excited about these flexible carbon nanotube fibers and their long-term biocompatibility.”
Weeks-long tests on cells and then in rats with Parkinson’s symptoms proved the fibers are stable and as efficient as commercial platinum electrodes at only a fraction of the size. The soft fibers caused little inflammation, which helped maintain strong electrical connections to neurons by preventing the body’s defenses from scarring and encapsulating the site of the injury.
The highly conductive carbon nanotube fibers also show much more favorable impedance—the quality of the electrical connection—than state-of-the-art metal electrodes, making for better contact at lower voltages over long periods, Kemere said.
The working end of the fiber is the exposed tip, which is about the width of a neuron. The rest is encased with a three-micron layer of a flexible, biocompatible polymer with excellent insulating properties.
The challenge is in placing the tips. “That’s really just a matter of having a brain atlas, and during the experiment adjusting the electrodes very delicately and putting them into the right place,” said Kemere, whose lab studies ways to connect signal-processing systems and the brain’s memory and cognitive centers.
Doctors who implant deep brain stimulation devices start with a recording probe able to “listen” to neurons that emit characteristic signals depending on their functions, Kemere said. Once a surgeon finds the right spot, the probe is removed and the stimulating electrode gently inserted. Rice carbon nanotube fibers that send and receive signals would simplify implantation, Vitale said.
The fibers could lead to self-regulating therapeutic devices for Parkinson’s and other patients. Current devices include an implant that sends electrical signals to the brain to calm the tremors that afflict Parkinson’s patients.
“But our technology enables the ability to record while stimulating,” Vitale said. “Current electrodes can only stimulate tissue. They’re too big to detect any spiking activity, so basically the clinical devices send continuous pulses regardless of the response of the brain.”
Kemere foresees a closed-loop system that can read neuronal signals and adapt stimulation therapy in real time. He anticipates building a device with many electrodes that can be addressed individually to gain fine control over stimulation and monitoring from a small, implantable device.
“Interestingly, conductivity is not the most important electrical property of the nanotube fibers,” Pasquali said. “These fibers are intrinsically porous and extremely stable, which are both great advantages over metal electrodes for sensing electrochemical signals and maintaining performance over long periods of time.”
Source: Rice Univ.