Deans' stroke musings

Changing stroke rehab and research worldwide now.Time is Brain!Just think of all the trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 493 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It's quite disgusting that this information is not available from every stroke association and doctors group.
My back ground story is here:

Monday, November 30, 2015

Vorapaxar for secondary stroke prevention: perspectives and obstacles

Have not heard of this before so this is strictly up to your doctor and hospital to decide on. Once they know about it after YOU tell them to investigate this. Pay it forward, we have to do the work that our stroke associations are completely failing at.

Serebruany V, Kim M, Fortmann S, Hanley D; Expert Review of Neurotherapeutics 1-6 (Nov 2015)

Vorapaxar, a novel antiplatelet thrombin protease-activated receptor 1 (PAR-1) inhibitor, has been evaluated in the successful TRA2P trial and failed TRACER trial. The drug is currently approved for post myocardial infarction and peripheral artery disease indications on top of clopidogrel and/or aspirin. The stroke data after vorapaxar are mixed, dominated with heavy excess of intracranial bleeding risks and slightly worsened second stroke rates, but show less primary ischemic strokes. Fortunately, these conflicting data do not belong purely to vorapaxar per se but rather, reflect unreasonably aggressive strategies, including predominantly triple antiplatelet therapy, utilized in both Trial to Assess the Effects of SCH 530348 in Preventing Heart Attack and Stroke in Patients with Arteriosclerosis (TRA2P) and especially in Thrombin-Receptor Antagonist Vorapaxar in Acute Coronary Syndromes (TRACER). The FDA-confirmed evidence strongly suggests that unique pharmacokinetics and a very mild'comfort zone'antiplatelet profile makes vorapaxar a good candidate for improved secondary stroke prevention. The outcome-driven, randomized trial should test head-to-head monotherapy with vorapaxar (Zontivity®) versus clopidogrel (Plavix®) and versus dipyridamole with very low dose aspirin (Aggrenox®). The advantages and potential pitfalls of such a trial are discussed in this article.

Watching what I can't do

On one of my walks this afternoon at work to get to 10,000 steps a young guy ahead of me stops by a tree and and jumps up to grab the tree branch above his head and starts doing pullups.
Failure points for me;
1. I can't jump at all, not even an inch off the ground.
2. I can't reach my left arm above my shoulder.
3. I can't open my left hand to grab anything, when holding my left arm above my head to try to grab a bar to do a dead mans hang, can never get the fingers to open at the same time.
4. No ability to move the body off the dead mans hang at all.

But I did find a tree with a branch at shoulder height so I now can do this again:

Apple tree stroke rehab


Data Scientists Create World’s First Therapeutic Venom Database

I'm sure our fucking failures of stroke associations will not do anything with this to see if any possibilities exist to treat stroke, prevent stroke or help with rehab. Your doctors won't even know this exists.
What about Draculin- bat saliva?

Draculin, Stroke Drug From Vampire Bats, Moves Closer to Circulation

Snake venom? 

Snake Venom Helps Hydrogels Stop the Bleeding

Intravenous Ancrod for Treatment of Acute Ischemic Stroke

Tick spit?

A tick’s spit leads to an entire lesson in blood clotting


Cardiovascular brings up 73 records.
Neuron contains 3 records.
Plaque contains 79 records.
Nitric oxide has 33 records.
Neuro contains 342 records.
Dopamine contains 6 records.
What other searches should your doctor be using?
Which ones does your doctor know about?  ANYTHING AT ALL?

What doesn’t kill you could cure you. A growing interest in the therapeutic value of animal venom has led a pair of Columbia University data scientists to create the first catalog of known animal toxins and their physiological effects on humans.
VenomKB, short for Venom Knowledge Base, summarizes the results of 5,117 studies in the medical literature describing the use of venom toxins as painkillers and as treatments for diseases like cancer, diabetes, obesity, and heart failure. Drawn from an automated analysis of the literature, VenomKB documents nearly 42,723 effects on the body. Though modern medicine makes use of only a small fraction of the toxins documented thus far, the researchers hope that the catalog will spur the discovery of new compounds and medical treatments.
“With this list we can take stock of what we know about venoms and their therapeutic effects” said Nicholas Tatonetti, an assistant professor of biomedical informatics at Columbia University Medical Center and a member of the Data Science Institute. “The questions now is: How can we use this information with other databases to discover new compounds and therapies?”
Tatonetti and Joseph Romano, a graduate student, searched on the term “venoms/therapeutic use” in a database of 22 million medical research papers. This produced a list of 5,117 venom-related studies whose results they summarized using a pair of computer algorithms. After cross-referencing toxins and drugs listed under multiple names and correcting other irregularities in the data, they found 42,723 unique mentions of venoms having a specific effect on the body. Their results are published in a companion study to Venom KB in the journal Scientific Data.
Venom’s capacity to heal is paradoxically linked to its fast-acting, lethal effects in the wild. Found in more than 173,000 species, venoms evolved over millions of years to target molecules that are often involved in disease. The toxic proteins and amino acids known as peptides that make up venom act on cell receptors and ion channels, controlling how cells behave.
By mimicking or altering how these toxins act on specific human cells, researchers can develop drugs that inhibit pain or treat diseases, often with fewer side effects than those of drugs already on the market.
About a dozen major drugs have emerged from this strategy so far, National Geographic magazine reported in 2013. One of the first, an anticoagulant called Arvin, gained favor in the late 1960s after a doctor discovered that ancrod, a protein found in the venom of the Malayan pit viper, could treat blood clots in the legs.
The widely used type 2 diabetes drug Byetta, is made from the toxin exenatide, found in the saliva of the venomous Gila monster, a lizard native to the United States and Mexico.
Another drug, bombesin, uses a toxin found in the skin of the venomous European fire-bellied toad to treat gastrointestinal disorders. Bombesin’s ability to bind to neuronal tumors has led to interest in developing a florescent version that could guide surgeons around the edges of a tumor.
Five compounds produced by the venomous cone snail have made it to clinical trials, including ziconotide, the generic term for an analgesic similar to morphine.
The Malayan pit viper, Gila monster, European fire-bellied toad, and cone snail account for about 18 percent of the 5,117 venom-related studies now catalogued in Venom KB. Yet there are 10 million or more venomous species that have yet to be studied. Zoltan Takacs, a toxinologist who earned his Ph.D. in evolutionary studies at Columbia, estimates there are 20 million venom toxins waiting to be screened.
Venom KB got its start after Romano approached Tatonetti, his thesis adviser, about studying medicinal uses of venom. Tatonetti suggested that Romano start looking through the venom database. To their surprise there was neither a database nor a list. Still modest in size, VenomKB is expected to grow more useful as researchers contribute more data. “With a large enough library we can screen for more effective, safer compounds,” said Romano.
Databases of compounds and their biological effects have been used in recent years to discover and develop new drugs as well as uncover problems with drugs already in use. Tatonetti and his colleagues mined a federal database of documented drug side effects, the FDA Adverse Event Reporting System (FAERS), and discovered that the interaction of the anti-depressant paroxetine, sold under the brand name Paxil, and the statin pravastatin, sold as Pravachol, could raise blood glucose levels in diabetic patients.
With VenomKB up and running, Tatonetti and Romano plan to contribute data of their own. Starting with samples of dried venom from the black mamba, they will perform experiments and explore new treatments for chronic pain, diabetes and heart disease.
Source: Columbia University

Warm Temperatures Worsen Cardiovascular Disease but not Diabetes Risk

Interesting premise that we are not challenging our 'thermal comfort zone' and thus more likely to develop cardiovascular disease. In mice at least.
I can just see shivering patients in the hospital being told that cold is good for your vascular system.
You might want to think twice before turning up that thermostat during the holidays. A new study led by UCSF researchers has found that mice who spend too much time in their thermal “comfort zone” while gorging on fatty foods more than double their risk of developing cardiovascular disease compared to mice who stayed cool while eating the same diet.
The findings suggest that the standard practice of housing mice at relatively cool temperatures may actually benefit the animals’ long-term health by keeping their metabolisms active. On the other hand, it could be an impediment for researchers trying to understand metabolic disease in humans, since we spend much of our time at carefully regulated “thermoneutrality” – the temperature at which our metabolisms don’t have to do any extra work to keep us warm.
“This has had a profound effect on how I look at results coming out of my own lab,” said study senior author Ajay Chawla, M.D., Ph.D., a professor at UCSF’s Cardiovascular Research Institute and the departments of physiology and medicine in UCSF’s School of Medicine. “I don’t believe anything until we do it again at thermoneutrality.”
There is ongoing debate in the research community about the best temperature for the health and comfort of laboratory mice. The National Research Council recommends housing mice between 20 and 26 degrees Celsius (68 to 79 degrees Fahrenheit), well below the animals’ thermoneutral zone, which is closer to 30 C (86 F).
Chawla, who studies the effects of cold on metabolism, became interested in whether the practice of housing mice at relatively chilly temperatures changed their risk of developing metabolic disease.
Nearly two decades of research show that diets high in LDL cholesterol trigger chronic vascular inflammation, aggravating the growth of atherosclerotic plaques and leading to heart disease. In recent years, studies have suggested heightened immune activity could also be responsible for the onset of insulin resistance, an early warning sign of diabetes.
In the new paper, published Nov 5 in the journal Cell Metabolism, Chawla’s team found that mice housed at 30 C and fed fatty diets developed inflammation much more rapidly and ended up with twice as many atherosclerotic plaques than those housed at the more typical 22 C. On the other hand, the heightened inflammation resulting from warmer housing conditions had no significant effect on insulin resistance, in sharp contrast with previous results linking the two.
“This was a big surprise,” Chawla said. “It could be that inflammation has less to do with diabetes than we thought.”
Chawla suspects that the chronic chill lab mice typically experience protects against chronic inflammation by constantly revving the metabolism to produce heat. The heart rate of a mouse at 22 C is typically twice as high as a mouse at 30 C, they expend twice as much energy at rest, and have significantly elevated blood pressure.
“The magnitude of the response is huge,” Chawla said. “We do all these studies on mice hoping to apply what we learn about mouse physiology to humans, but it’s like we’ve been studying humans on speed.”
Source: University of California San Francisco

Sunday, November 29, 2015

Mayo Clinic high blood pressure DVD

Wow, even the Mayo clinic has been compromised with Complementary and Integrative medicine. Lots of woo in that dvd. Yoga and meditation are not complementary, they are evidence based and so are real medicine. No real help with nutrition in there. Can't tell how old this is but it still has the main restrictions on salt, which is in dispute right now. I'm obviously totally unbalanced at least according to their medicine wheel quadrants; physical, mental, emotional, spiritual. I have no spiritual beliefs so my three spoked wheel has to compensate. It's doing a damn good job.

7 Brain Benefits of Turmeric Derivative J147

Would this help us post-stroke? We'll never know because we have no one to go to to ask such fuckingly simple questions. Don't try this on your own, you know how dangerous tumeric is. Millions of Indians probably use it daily and they obviously don't understand the risk they are taking by not having it doctor prescribed. It is only tested in mice. You will have to ask your doctor if this is better than getting transfusions of young blood.
Salk Institute's J147 is a derivative of turmeric, a spice used in curry. Learn how it quickly reverses memory deficits and has a host of unexpected anti-aging effects in the lab.

7 Benefits

The old mice fed J147 saw the following benefits:
  1. They performed better on memory and other tests for cognition
  2. They displayed more robust motor movements.
  3. They had fewer pathological signs of Alzheimer's in their brains.
  4. J147 prevented the leakage of blood from the microvessels in the brains of old mice. "Damaged blood vessels are a common feature of aging in general, and in Alzheimer's, it is frequently much worse," says Currais.

    Importantly, because of the large amount of data collected on the three groups of mice, it was possible to demonstrate that many aspects of gene expression and metabolism in the old mice fed J147 were very similar to those of the young animals. These included:
  5. markers for increased energy metabolism,
  6. reduced brain inflammation and
  7. reduced levels of oxidized fatty acids in the brain.

Human Clinical Trials

Currais and Schubert note that while these studies represent a new and exciting approach to Alzheimer's drug discovery and animal testing in the context of aging, the only way to demonstrate the clinical relevance of the work is to move J147 into human clinical trials for Alzheimer's disease.

"If proven safe and effective for Alzheimer's, the apparent anti-aging effect of J147 would be a welcome benefit," adds Schubert. The team aims to begin human trials next year.

Can a flickering light predict dementia, diagnose it and measure its progress?

The article about it here:
The actual research here, behind a paywall:

Critical Flicker Fusion Predicts Executive Function in Younger and Older Adults

Kicking Back Cognitive Ageing: Leg Power Predicts Cognitive Ageing after Ten Years in Older Female Twins

Our physical therapists should be able to translate this into a stroke protocol. It took me years to be able to walk enough to get winded. So we should be able to change this to rowing or biking machines while still in the hospital. But I bet this won't occur in any hospital in the world, because we have nothing for stroke associations. You're screwed once again unless YOU have enough cognitive power to read all the relevant research and plan your own recovery.

Steves C.J.a, b · Mehta M.M.c · Jackson S.H.D.b · Spector T.D.a, b
aDepartment of Twin Research and Genetic Epidemiology, Kings College London, bDepartment of Clinical Gerontology, Kings College Hospital, and cCentre for Neuroimaging Sciences, Institute of Psychiatry, Kings College London, London, UK email Corresponding Author


Background: Many observational studies have shown a protective effect of physical activity on cognitive ageing, but interventional studies have been less convincing. This may be due to short time scales of interventions, suboptimal interventional regimes or lack of lasting effect. Confounding through common genetic and developmental causes is also possible. Objectives: We aimed to test whether muscle fitness (measured by leg power) could predict cognitive change in a healthy older population over a 10-year time interval, how this performed alongside other predictors of cognitive ageing, and whether this effect was confounded by factors shared by twins. In addition, we investigated whether differences in leg power were predictive of differences in brain structure and function after 12 years of follow-up in identical twin pairs.  
Methods: A total of 324 healthy female twins (average age at baseline 55, range 43-73) performed the Cambridge Neuropsychological Test Automated Battery (CANTAB) at two time points 10 years apart. Linear regression modelling was used to assess the relationships between baseline leg power, physical activity and subsequent cognitive change, adjusting comprehensively for baseline covariates (including heart disease, diabetes, blood pressure, fasting blood glucose, lipids, diet, body habitus, smoking and alcohol habits, reading IQ, socioeconomic status and birthweight). A discordant twin approach was used to adjust for factors shared by twins. A subset of monozygotic pairs then underwent magnetic resonance imaging. The relationship between muscle fitness and brain structure and function was assessed using linear regression modelling and paired t tests.  
Results: A striking protective relationship was found between muscle fitness (leg power) and both 10-year cognitive change [fully adjusted model standardised β-coefficient (Stdβ) = 0.174, p = 0.002] and subsequent total grey matter (Stdβ = 0.362, p = 0.005). These effects were robust in discordant twin analyses, where within-pair difference in physical fitness was also predictive of within-pair difference in lateral ventricle size. There was a weak independent effect of self-reported physical activity.  
Conclusion: Leg power predicts both cognitive ageing and global brain structure, despite controlling for common genetics and early life environment shared by twins. Interventions targeted to improve leg power in the long term may help reach a universal goal of healthy cognitive ageing.

Saturday, November 28, 2015

Being ever more productive… is a duty - But not for stroke

And yet our stroke medical professionals and stroke associations are completely failing us in this regard.
I'll highlight a couple key lines;
If you are treating medical conditions for the same cost and getting the same results for the last few years, you are stealing from all of us.
You have an obligation to improve your productivity with each passing year. And only if all of us keep on improving our productivity can we afford to grow everyone’s budget year after year.

Smoking high-strength cannabis may damage nerve fibres in brain

But is it the smoking that does this or the marijuana? Easy to find out, just injest the same strength and test what happens. This result will not change my use after my next stroke.
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 

 Smoking high-strength cannabis may damage nerve fibres in brain
High-strength cannabis may damage nerve fibres that handle the flow of messages across the two halves of the brain, scientists claim. Brain scans of people who regularly smoked strong skunk-like cannabis revealed subtle differences in the white matter that connects the left and right hemispheres and carries signals from one side of the brain to the other.
The changes were not seen in those who never used cannabis or smoked only the less potent forms of the drug, the researchers found.

The study is thought to be the first to look at the effects of cannabis potency on brain structure, and suggests that greater use of skunk may cause more damage to the corpus callosum, making communications across the brain’s hemispheres less efficient.
Paola Dazzan, a neurobiologist at the Institute of Psychiatry at King’s College London, said the effects appeared to be linked to the level of active ingredient, tetrahydrocannabinol (THC), in cannabis. While traditional forms of cannabis contain 2 to 4 % THC, the more potent varieties (of which there are about 100), can contain 10 to 14% THC, according to the DrugScope charity.
“If you look at the corpus callosum, what we’re seeing is a significant difference in the white matter between those who use high potency cannabis and those who never use the drug, or use the low-potency drug,” said Dazzan. The corpus callosum is rich in cannabinoid receptors, on which the THC chemical acts.

“The difference is there whether you have psychosis or not, and we think this is strictly related to the potency of the cannabis,” she added. Details of the study are reported in the journal Psychological Medicine.
The researchers used two scanning techniques, magnetic resonance imaging (MRI) and diffusion tensor imaging (DTI), to examine the corpus callosum, the largest region of white matter, in the brains of 56 patients who had reported a first episode of psychosis, and 43 healthy volunteers from the local community.
The scans found that daily users of high-potency cannabis had a slightly greater – by about 2% – “mean diffusivity” in the corpus callosum. “That reflects a problem in the white matter that ultimately makes it less efficient,” Dazzan told the Guardian. “We don’t know exactly what it means for the person, but it suggests there is less efficient transfer of information.”
The study cannot confirm that high levels of THC in cannabis cause changes to white matter. As Dazzan notes, it is may be that people with damaged white matter are more likely to smoke skunk in the first place.
“It is possible that these people already have a different brain and they are more likely to use cannabis. But what we can say is if it’s high potency, and if you smoke frequently, your brain is different from the brain of someone who smokes normal cannabis, and from someone who doesn’t smoke cannabis at all,” she said.

But even with the uncertainty over cause and effect, she urged users and public health workers to change how they think about cannabis use. “When it comes to alcohol, we are used to thinking about how much people drink, and whether they are drinking wine, beer, or whisky. We should think of cannabis in a similar way, in terms of THC and the different contents cannabis can have, and potentially the effects on health will be different,” she said.
“As we have suggested previously, when assessing cannabis use, it is extremely important to gather information on how often and what type of cannabis is being used. These details can help quantify the risk of mental health problems and increase awareness of the type of damage these substances can do to the brain,” she added.
In February, Dazzan and others at the Institute of Psychiatry reported that the ready availability of skunk in south London might be behind a rise in the proportion of new cases of psychosis being attributed to cannabis.

The visual amplification of goal-oriented movements counteracts acquired non-use in hemiparetic stroke patients

I bet this never makes it to your stroke department because we have no organization that rolls out new research to all stroke doctors and hospitals.  Expecting all the doctors and hospitals in the world to keep up and translate research into actionable protocols is an exercise in stupidity. Has your doctor EVER told you of new research they just read that changed your stroke protocols? Does your doctor read research?
  • Belén Rubio BallesterEmail author,
  • Jens Nirme,
  • Esther Duarte,
  • Ampar Cuxart,
  • Susana Rodriguez,
  • Paul Verschure and
  • Armin Duff
Journal of NeuroEngineering and Rehabilitation201512:50
DOI: 10.1186/s12984-015-0039-z
Received: 5 February 2015
Accepted: 13 May 2015
Published: 9 June 2015



Stroke-induced impairments result from both primary and secondary causes, i.e. damage to the brain and the acquired non-use of the impaired limbs. Indeed, stroke patients often under-utilize their paretic limb despite sufficient residual motor function. We hypothesize that acquired non-use can be overcome by reinforcement-based training strategies.


Hemiparetic stroke patients (n = 20, 11 males, 9 right-sided hemiparesis) were asked to reach targets appearing in either the real world or in a virtual environment. Sessions were divided into 3 phases: baseline, intervention and washout. During the intervention the movement of the virtual representation of the patients’ paretic limb was amplified towards the target.


We found that the probability of using the paretic limb during washout was significantly higher in comparison to baseline. Patients showed generalization of these results by displaying a more substantial workspace in real world task. These gains correlated with changes in effector selection patterns.


The amplification of the movement of the paretic limb in a virtual environment promotes the use of the paretic limb in stroke patients. Our findings indicate that reinforcement-based therapies may be an effective approach for counteracting learned non-use and may modulate motor performance in the real world.

Treatment of Brain AVMs (TOBAS): study protocol for a pragmatic randomized controlled trial

In case you have an AVM and want to know the latest. Might still be going if interested.
Tim E. Darsaut1, Elsa Magro23, Jean-Christophe Gentric45, André Lima Batista4, Chiraz Chaalala2, David Roberge6, Michel W. Bojanowski2, Alain Weill4, Daniel Roy4 and Jean Raymond4*
1 Department of Surgery, Division of Neurosurgery, University of Alberta Hospital, Mackenzie Health Sciences Center, Edmonton, AB, Canada
2 Department of Surgery, Service of Neurosurgery, Centre Hospitalier de l’Université de Montréal (CHUM), Notre-Dame Hospital, Montreal, QC, Canada
3 Service de Neurochirurgie, CHU Cavale Blanche, INSERM UMR 1101 LaTIM, Brest, France
4 Department of Radiology, Service of Neuroradiology, Centre Hospitalier de l’Université de Montréal (CHUM), Notre-Dame Hospital, Interventional Neuroradiology (NRI), 1560 Sherbrooke East, Pavillion Simard, room Z12909, Montreal H2L 4 M1, QC, Canada
5 Service de Radiologie, CHU Cavale Blanche, Brest, EA 3878 GETBO, France
6 Department of Radio-Oncology, Centre Hospitalier de l’Université de Montréal (CHUM), Notre-Dame Hospital, Montreal, QC, Canada
For all author emails, please log on.
Trials 2015, 16:497  doi:10.1186/s13063-015-1019-0
The electronic version of this article is the complete one and can be found online at:

Received:8 December 2014
Accepted:20 October 2015
Published:4 November 2015
© 2015 Darsaut et al.

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (, which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( applies to the data made available in this article, unless otherwise stated.



The management of unruptured brain arteriovenous malformation (AVM) patients remains controversial. Furthermore, curative attempts to treat ruptured AVM patients have not been questioned so far, and there is a lack of prospective data on clinical results according to treatment modality. Endovascular treatment is often used aiming to improve the safety or efficacy of surgery or radiation therapy, but benefits have never been documented in a trial. A care trial context is needed to evaluate interventions at the same time they are practised.

Methods/Trial design

TOBAS is a pragmatic, prospective, multicenter, randomized, controlled trial and registry which offers a care trial context for brain AVM patients, including surgical resection, radiosurgery or endovascular embolization, alone or combined. The study includes two RCTs and a multimodality prospective registry. The objectives of the proposed study are to assess whether preventive interventions (surgery, embolization, radiation therapy, alone or combined), selected by the local treatment team and performed as locally practiced, randomly allocated and compared with conservative management, in unruptured brain AVM patients eligible for active or conservative management, can improve the proportion of patients having an independent outcome (modified Rankin Scale (mRS) < 3, as assessed by a standardized questionnaire administered by non-masked care personnel) at 10 years. All patients judged ineligible for randomized allocation are to be entered in a multimodal registry. The objective of a nested trial in patients with ruptured or unruptured AVMs to be treated by surgery or radiation therapy, is to assess whether pre-surgical or pre-radiation embolization, randomly allocated and compared with no embolization, can improve the proportion of patients with complete eradication of the AVM, as locally adjudicated, combined with a good clinical outcome (mRS < 3). The study will require up to 2000 patients in approximately 30 centers or more, followed for 10 years. TOBAS is registered at NCT02098252 as of 25 March 2014. 

Trial status

TOBAS is currently recruiting patients in one Canadian center, and the protocol is under ethics board review at other national and international sites. To date, 80 patients have been recruited. 

More at link.

More neurons mean less need for sleep

Do you still have enough neurons to not need as much sleep? Has your doctor tested for this and adjusted your sleep protocol? Do you have ANY PROTOCOLS AT ALL? 
Vol. 350 no. 6264 p. 1052
DOI: 10.1126/science.350.6264.1052-a
  • Editors' Choice

More neurons mean less need for sleep

Species with more neurons, such as this Gelada baboon, may need less sleep
Sleep is seemingly universal among animals. Daily sleep time varies considerably between mammalian species and also during mammalian development, yet we still don't know what drives this variation. Herculano-Houzel hypothesized that sleep-inducing metabolites produced during waking hours accumulate more slowly in brains that have a smaller density of neurons underneath a unit surface area that gets washed by cerebrospinal fluid during waking. In 24 mammalian species and several postnatal stages in the developing rat, there was indeed a correlation between the ratio of neuronal density to brain surface area and daily sleep duration. The evolutionary addition of neurons may have decreased the need for sleep, allowing a species to feed for longer, and thus facilitated further increases in neuronal numbers.
Proc. R. Soc. London Ser. B 282, 1816 (2015).

Friday, November 27, 2015

Fewer Heart Attacks With Mind–Body Medicine - Stroke???

Whom is going to do the research like this on stroke? Don't worry, it will never get done.

Mind–body medicine (MBM) is a holistic approach that has the potential to ward off more heart attacks than conventional prevention programs. That is the conclusion reached by Holger Cramer and colleagues in a systematic review and meta-analysis presented in the latest issue of Deutsches Ärzteblatt International (Dtsch Arztebl Int 2015; 112: 759-67). They show that MBM in cardiac patients has a positive effect on coronary events, atherosclerosis, and high blood pressure.
Three of the most important risk factors for coronary heart disease—lack of exercise, overweight, and stress—are amenable to intervention. While conventional preventive measures concentrate on exercise and advice on nutrition, MBM also embraces relaxation methods and psychological motivation techniques. In the studies analyzed by Cramer et al., coronary events occurred in 68 of 307 patients who received conventional interventions but in only half as many—33/308—of those on MBM prevention programs. The authors point out that despite this positive effect MBM does not decrease mortality in cardiac patients. Nevertheless, the lower incidence of coronary events is beneficial. They therefore endorse MBM or other comparable programs for lifestyle modification.

Top priorities named in hearing loss research - Stroke???

What the fuck are the top priorities in stroke research? Do we even know what we should be researching? Or is this just a crapshoot hoping to find something useful? A great stroke association would have a defined strategy on what research should be funded next in order to solve all the fucking problems in stroke.
Experts have published a list of the most urgent priorities for researching a debilitating condition that affects more than 10 million people in the UK.
Published in The Lancet, the top 10 research priorities for tackling mild to moderate hearing loss aims to re-focus future studies on areas which could potentially have the greatest impact in furthering understanding of the condition and developing successful new treatments.
Co-author Dr Helen Henshaw, a University of Nottingham academic based at the National Institute for Health Research (NIHR) Nottingham Hearing Biomedical Research Unit, said: “Although hearing loss is not deadly, it can have a profound impact on people’s ability to maintain relationships, lead a normal life and go out to work.
“With such a huge proportion of the population affected by this condition, it is vital that hearing research funding is prioritised for the questions which are most important to them.”
Despite being one of the six health priority areas for the NIHR, significantly less is spent on hearing research – just £47 per one lost year of healthy life compared to other priority conditions such as sight loss (£99) and diabetes (£399).
Currently, evidence which underpins clinical practice is typically provided by researchers in universities that are far-removed from frontline clinical services and which often does not take into account the views and experiences of key stakeholders.
The list of Top 10 hearing loss priorities were identified by an innovative partnership, the James Lind Alliance, which brings together patients, carers and clinicians to identify the unanswered questions about the effects of treatments that they agree are the most important.
It canvassed the views of more than 460 people on what they believed were the most significant treatment uncertainties before asking them to rank the importance of more than 80 research questions connected to these areas on a scale of importance. The top 30 ranked questions were then taken forward to a final prioritisation workshop, which then narrowed these down to the final top 10 based on consensus from a group of patients, family, friends and clinicians.
The final top 10 includes questions about the prevention (or cure), diagnosis and treatment, with the majority of treatment questions concerned with aspects of hearing aid provision.
All of the uncertainties identified by the James Lind Alliance Priority Setting Partnership, including the top 10, will be uploaded to the Database of Uncertainties About the Effects of Treatments to be made widely to the public, the research community, research commissioners and research funders.
The project was supported by funding awarded by the Nottingham University Hospitals Charity and the National Institute for Health Research Biomedical Research Unit Programme.
Full bibliographic informationHelen Henshaw, Linda Sharkey, David Crowe, Melanie Ferguson; Research priorities for mild-to-moderate hearing loss in adults;
The Lancet Vol 386 November 28, 2015;

All-female team merges high tech and high touch to serve stroke survivors - smartphone monitoring

This makes a lot of sense except that lots of survivors are one-handed and use that hand to get various body parts into the correct position. But better than nothing.
Three professors at Towson University have developed a mobile app called ARMStrokes that allows stroke survivors to use a smart phone to perform their rehab exercises anywhere.
Stroke is a major contributor to adult disability in many countries. According to the Centers for Disease Control and Prevention, more than 795,000 people in the United States have a stroke each year. Stroke often causes long-term disabilities that affect cognitive, physical, and speech functions. Prompt and intensive rehabilitation exercise is critical for stroke recovery. However, only 31 percent of stroke survivors actually complete recommended exercise due to a variety of factors, including issues of accessibility and lack of motivation.
Smartphones are easily accessible and can be carried anyplace. They also do not require complicated installation or configuration processes, and can serve as a resource for learning and entertainment. With the proper app, smartphones can be used as a rehabilitation platform. Individuals can play rehabilitation games delivered through mobile phones while watching TV, relaxing in the park, or even waiting in line in a grocery store. In addition to the benefit of easy access, the mobile phone can also support timely communication between stroke survivors, therapists and their caregivers, so that compliance to in-home exercise programs and progress can be monitored effectively.
“Since the functionality of stroke patients varies dramatically, ARMStrokes can be easily customized to fit each stroke survivor’s specific functionalities in different recovery stages,” says Dr. Sonia Lawson who works in the area of adult neurological conditions and stroke rehabilitation in the Department of Occupational Therapy and Occupational Science. Completing the interdisciplinary team is Dr. Katherine Tang and Dr. Heidi Feng, who are both members of the Department of Computer and Information Sciences faculty. Dr. Tang’s research focuses on multimedia and game design. Dr. Feng is an expert in assistive technologies, human computer interaction and health informatics.
During each exercise session, the app guides the user through a series of gross motor movements (movements that use the large muscles in the arms, legs, torso and feet) and provides visual, audio and haptic feedback, usually in the form of phone vibrations, according to the quality of the movement performed.
Figure 2. Screenshots for daily goals and calibration settings.
Figure 2. Screenshots for daily goals and calibration settings.
ARMStrokes supports several arm motions such as shoulder flexion, abduction, elbow flexion and extension, and forearm pronation/supination. Built-in smartphone sensors detect the excursion of movements – number of repetitions and degree of movement – and transmit the data to a secured server. With a password, a therapist, caregiver or user can access the secured data server via a website to track performance and progress over time and improve therapy outcomes. The therapist can also make modifications to exercise programs remotely through the secure network.
The research team is conducting a field study in collaboration with the University of Maryland Rehabilitation and Orthopaedic Institute to evaluate the app without patients.
The project is supported by both the Aetna Foundation and the School of Emerging Technologies at Towson University. More information about the project is available at

A census of neocortical neurons

How many types of neurons does your doctor know about and what are the different stroke protocols to rebuild/recover them?
Vol. 350 no. 6264 pp. 1051-1053
DOI: 10.1126/science.350.6264.1051-l
  • This Week in Science

A census of neocortical neurons

Despite the importance of the brain's neocortex, we still do not completely understand the diversity and functional connections of its cell types. Jiang et al. recorded, labeled, and classified over 1200 interneurons and more than 400 pyramidal neurons in the mature mouse visual cortex. Fifteen major classes of interneurons fell into three types: some connect to all neurons, some connect to other interneurons, and some form synapses with pyramidal neurons.
Science, this issue p. 10.1126/science.aac9462

High-fat diet appears to prompt immune cells to start consuming connections between neurons

It this doesn't cause your doctor, hospital and stroke association to create a stroke diet protocol, you've got idiots in charge. We can't lose any more neuron connections. Remember no prescribing this on your own, you know how dangerous eating on your own is. Of course this is in mice so that will be their excuse. No clinical human studies have been done.
When a high-fat diet causes us to become obese, it also appears to prompt normally bustling immune cells in our brain to become sedentary and start consuming the connections between our neurons, scientists say.
The good news is going back on a low-fat diet for just two months, at least in mice, reverses this trend of shrinking cognitive ability as weight begins to normalize, said Dr. Alexis M. Stranahan, neuroscientist in the Department of Neuroscience and Regenerative Medicine at the Medical College of Georgia.
"Microglia eating synapses is contributing to synapse loss and cognitive impairment in obesity," Stranahan said. "On the one hand, that is very scary, but it's also reversible, meaning that if you go back on a low-fat diet that does not even completely wipe out the adiposity, you can completely reverse these cellular processes in the brain and maintain cognition."
Stranahan is corresponding author of the study in the journal Brain, Behavior, and Immunity, which provides some of the first evidence of why fat is bad for the brain.
The trouble appears to start with too much fat in the body producing chronic inflammation, which stimulates microglia to have an autoimmune response. Microglia, like macrophages in the body, are known for their ability to ingest trash and infectious agents in the brain, and their highly acidic interior gets rids of it, which helps support the function and health of neurons. But as mice get obese, their microglia seem focused on overeating.
"Normally in the brain, microglia are constantly moving around. They are always moving around their little fingers and processes. What happens in obesity is they stop moving," Stranahan said. "They draw in all their processes; they basically just sit there and start eating synapses. When microglia start eating synapses, the mice don't learn as effectively," Stranahan said.
The study looked at normal male mice: One group ate a diet in which about 10 percent of the calories came from saturated fat, and another consumed chow that was 60 percent fat. To ensure other factors were equal, the researchers chose chows that had similar levels of other key ingredients such as macronutrients and protein. The chows were on par with a healthy diet versus a fast-food diet in humans. "If you look at the lipid breakdown for the two diets, these guys are getting crazy, crazy amounts," Stranahan said of the high-fat-fare mice.
At four, eight and 12 weeks, the MCG scientists took a series of metabolic measures, such as weight, food intake, insulin and serum glucose levels. They also measured in the hippocampus, the center of learning and memory, levels of synaptic markers, proteins found at synapses that correlate with the number of synapses.
"This gives us a window into what is occurring at the level of the synapse and also microglial activation," Stranahan said. And, they measured levels of inflammatory cytokines, which microglia produce when "they start getting activated and angry."
All levels in both groups were essentially the same at four weeks. The mice on a high-fat diet were fatter, but other measures were normal at eight weeks. By 12 weeks the fat-eating mice were obese, had elevated cytokine levels and a reduction in the markers for synapse number and function.
"When you get out to 12 weeks, you start seeing great increases in peripheral obesity. While you don't see insulin resistance, you also start seeing loss of synapses and increases in inflammatory cytokines in the brain," Stranahan said.
At that point, the research team switched half the mice on the high-fat diet to the low-fat regimen. It took about two months for their weight to return to normal, although their overall fat pad remained larger than their peers who had never gained weight. That fat layer makes it easier to gain weight in the future, Stranahan notes. As with most people, the mice that remained on the low-fat diet slowly accumulated a little weight as they aged.
Meanwhile, the group that stayed on the high-fat diet kept getting fatter, more inflamed and losing synapses, she said. Their microglia's little processes, or protrusions, which normally help monitor synaptic function and help these cells move, continued to wither. Dendritic spines on neurons, which get input from synapses, similarly withered on the high-fat diet, but like the microglia processes, were restored with the lower-fat fare.
"That is very promising," said Stranahan. The findings also point to some potential new purposes for existing drugs now used for conditions such as rheumatoid arthritis and Crohn's disease, which block specific inflammatory cytokines and tumor necrosis factor alpha, both of which are elevated in the brains of the fat mice.
Obesity yields extreme overkill in microglia, which are typically extremely discriminating and helpful to neurons. During development, for example, they will prune a synapse that isn't functioning. "That is one way the developing brain refines itself. It allows you to keep only those synapses that you need or the synapses you have been using. Fat dramatically alters their dynamic.
"Instead of doing garbage disposal, they are taking your mailbox, your front door, your kitchen sink and all the stuff that you need, and not doing their job of getting rid of trash," Stranahan said.
She notes that the high-fat-eating mice actually ate less chow and consumed the same amount of calories as mice eating low fat. "The entire metabolic phenotype is driven by diet composition rather than the amount of calories," Stranahan said. If high-fat-eating mice had greater variety in their diet, such as a sugar-water option, they might also consume more total calories, similar to the sensory-specific satiety phenomenon in humans, she said.
Medical College of Georgia at Georgia Regents University

Thursday, November 26, 2015

Young Women Who Survive Cardiovascular Event Have Long-Term Risks

Be careful out there.
Young women who survive a myocardial infarction (MI) or a stroke still face long-term risks of death and illness, according to a study published online by JAMA Internal Medicine.
While death rates from the acute phase of cardiovascular events have decreased, the disease burden remains high in the increasing number of survivors, which is especially important for those affected at a young age. However, little information is available about the long-term outcomes of young patients, especially women, who survive cardiovascular events.
For the current study, Frits R. Rosendaal, MD, Leiden University Medical Center, Leiden, the Netherlands, and colleagues determined long-term mortality and morbidity in young women who survived a MI or an ischaemic stroke and compared them with a control group.
The study included 226 women who had a MI (mean age, 42 years), 160 women who had an ischaemic stroke (mean age, 40 years), and 782 women (mean age, 48 years) in the comparison group with no history of arterial thrombosis. The women were followed-up for a median of nearly 19 years.
Death rates were 3.7 times higher in women who had a MI (8.8 per 1,000 person-years) and 1.8 times higher in women who had an ischaemic stroke (4.4 per 1,000 person-years) compared with the control group (2.4 per 1,000 person-years). This elevated mortality lasted over time and was mainly supported by a high rate of deaths from acute vascular events.
When both fatal and nonfatal cardiovascular events were counted, the incidence rate was highest in women who had an ischaemic stroke (14.1 per 1,000 person-years) compared with the control group. The rate was 12.1 per 1,000 person-years in women who had a MI.
In women who had a MI, the risk of cardiac events was 10.1 per 1,000 person-years and the risk of cerebral events was 1.9 per 1,000 person-years. In women who had an ischaemic stroke, the risk of cerebral events was 11.1 per 1,000 person-years and the risk of cardiac events was 2.7 per 1,000 person-years.
The authors acknowledge a reduced generalisability of their results because procedures and risk factors change over time, which is a problem of all long-term follow-up studies.
“Our findings provide direct insight into the consequences of cardiovascular diseases in young women, which persist for decades after the initial event, stressing the importance of life-long prevention strategies,” the authors concluded.
SOURCE: JAMA Internal Medicine

The Science of Ischemic Stroke: Pathophysiology & Pharmacological Treatment

This person has done a wonderful job of  consolidating practically everything that needs to  be done in stroke in 20 pages with 127 references. If your doctor is not conversant in all this s/he should be fired.
This diagram from there should be a great start on establishing what research should be sponsored to solve a lot of the problems with the neuronal cascade of death. If our stroke associations don't do something with this they should all be fired and be replaced with something else, maybe persons with functioning brains.
Figure 1 on page 4

Damn it all, the direction to go is established. Someone just needs to get foundation grants to sponsor research to find the answers.

Ultrasound examinations can identify patients at risk of stroke

But wouldn't it be better to know if you have the unstable kind of plaque that is highly suggestive of risk of stroke?

New research allows doctors to image dangerous ‘hardening’ of the arteries

In fact, this new emerging technique is the only imaging platform that can non-invasively detect the early stages of calcification in unstable atherosclerosis.”


Ultrasound examinations can identify patients at risk of stroke
Ultrasound, a non-invasive technique commonly used to study the presence of atherosclerosis disease in blood vessels, can be used to identify patients at increased risk of future stroke who could benefit from surgery. Since surgical treatment to prevent stroke is only considered beneficial to some, ultrasound can prove useful in preventing unnecessary surgical intervention, new research at Umeå University in Sweden shows.
Atherosclerosis, or hardening of the arteries, is an inflammatory disease affecting the arteries supplying the brain, heart, other organs and extremities with oxygen-rich blood. A well-established atherosclerosis disease, with accumulation of plaque narrowing the arteries, can obstruct the blood supply to the brain and other vital organs. Atherosclerosis in the neck arteries can cause stroke. The serious condition, known as carotid stenosis, is quite common in the elderly as well as in people with risk factors such as hypertension, smoking, diabetes, hypercholesterolemia and obesity.
Atherosclerosis disease progression can be controlled by medical treatment including cholesterol-lowering drugs, and significant narrowing in symptomatic patients can be treated surgically.
“We know that preventive surgical treatment of carotid stenosis is only beneficial for a small subgroup, and that most asymptomatic patients will do better with only medical therapy. By using ultrasound, we can identify the patients who are at a higher risk of stroke and thus would benefit from surgery. But preventing unnecessary surgical intervention in most cases is equally important,” says Fisnik Jashari, doctoral student at the Department of Public Health and Clinical Medicine and author of the dissertation.
To assess the nature of atherosclerosis disease and the extent of plaque build-up, the non-invasive ultrasound method remains favoured over most others because it is radiation free, cheap and patient-friendly.
Fisnik Jashari comes from Prishtina in Kosovo, where he works as resident doctor in Neurology. He is a doctoral student in the Department of Public Health and Clinical Medicine at Umeå University.

Therapeutic Hypothermia Saves Neurological Functions After Cardiac Arrest

But what about stroke survivors? I've written 30 posts on this with conflicting results. Which way is your doctor and hospital leaning? Any stroke protocol at all? You'll have to ask ahead of time since you may not be in cognitive shape to ask for it in the middle of your stroke. And they would need the cooling implements already at the hospital unless it is winter and they can toss you in a snowbank.
Survivors of cardiac arrest who remain in comas have better survival and neurological outcomes when their body temperatures are lowered, according to a study published in the journal Circulation.
Previous studies have shown the therapy effective on patients with shockable heart rhythms like ventricular fibrillation. However, the current study demonstrates that it’s also effective on patients with non-shockable rhythms when there is no pulse and the patient is in a coma.
“Prior to our study, there was minimal data to support the use of this treatment on patients with non-shockable rhythms,” Sarah Perman, MD, University of Colorado School of Medicine, Aurora, Colorado. “As a result, the therapy was not widely used with these patients.”
For the study, the researchers looked at data from 519 patients who had non-shockable heart rhythms between 2000 and 2013. They found that those who received therapeutic hypothermia were 2.8 times as likely to survive to be discharged from the hospital and 3.5 times more likely to have better neurological outcomes (returning to their baseline mental state) than those who did not have the treatment.
Physicians who use the technique employ cooling wraps to drop the patients' temperature from approximately 37 degrees Celsius to 33 degrees Celsius. The therapy has shown to reduce damage to the brain following a cardiac arrest, though scientists continue to investigate why this occurs.
Landmark trials in 2002 studying shockable patients found that 49% of those who received therapeutic hypothermia had good neurological outcomes as opposed to 26% who did not receive the treatment. Another trial showed 55% of patients with good neurological outcome against 39% who didn’t have the therapy.
“Neurologic injury after cardiac arrest is devastating,” said Dr. Perman. “We have one chance to give some form of neuroprotection, and that's immediately after the arrest.”
She said therapeutic hypothermia should be more widely used in comatose patients to protect neurological function.
“We know that patients benefit from this therapy,” said Dr. Perman, noting the importance of delivering meaningful research from the laboratory directly to the patient. “Therefore, one of our next challenges is to tailor the hypothermia treatment to the patient’s specific injury in order to improve outcomes further.”
SOURCE: University of Colorado Anschutz Medical Campus

Does soy reduce cholesterol?

You'll have to scour the American Heart Association site to find the research because I hate these articles that don't directly point to research. And this is from the Mayo Clinic.
Possibly. Although eating soy-based foods can slightly reduce your low-density lipoprotein (LDL, or "bad") cholesterol level, the American Heart Association has concluded that soy doesn't significantly lower cholesterol.
However, eating soy-based foods can still be good for you because soy-based foods contain less saturated fat than meat does and also provide other beneficial nutrients, such as vitamins, minerals and fiber
If you substitute soy for animal-based products, this switch — rather than the soy itself — may reduce your cholesterol.
Talk to your doctor or dietitian if you're interested in adding more soy to your diet.
 (I doubt this will help one bit because your doctor had almost zero training in nutrition)

Neuroprotection by the soy isoflavone, genistein, via inhibition of mitochondria-dependent apoptosis pathways and reactive oxygen induced-NF-κB activation in a cerebral ischemia mouse model

Only three years old and I bet your doctor and hospital have not done one fucking thing to help your recovery based upon this research. What is the downside even though this is only in mice? Are your doctors waiting for clinical human studies before they do anything? Stroke survivors will never get better if we don't have any doctors willing to show some initiative and try new stuff based upon research. They can have you sign a waiver stating you won't sue them for feeding you soybeans. So much that can be done for survivors and no one even trying to help them. And you wonder why I'm angry all the time. I fucking hate stupid people. Lazy people even more.
But this might be difficult because you have to know 14 days before your stroke so you can start pretreatment. This would then require research showing if this is helpful treating poststroke. So much research to do and no one to do it.
Qian Y, et al. Neurochem Int. 2012.


Recently, the treatment of stroke has focused on antioxidant therapies, where oxidative stress is implicated. The preventive and therapeutic potential of plant compounds on ischemic stroke has been intensively studied because many of them contain antioxidant properties. Genistein, one of the active ingredients in soybean, possesses many bioactivities. In this study, we investigated the potential neuroprotective effects of genistein and its possible mechanism of action in a cerebral ischemia mouse model. Mice were pretreated with genistein (2.5, 5, and 10mg/kg) or vehicle orally once daily for 14 consecutive days before transient middle cerebral artery occlusion was performed. Genistein at doses of 2.5-10mg/kg significantly reduced the infarct volume, improved the neurological deficit and prevented cell apoptosis after ischemia. In addition, genistein pretreatment was shown to inhibit the ischemia-induced reactive oxygen species (ROS) production, enhance the activities of antioxidant enzymes superoxide dismutase (SOD) and glutathione peroxidase (GPx), and decrease levels of malondialdehyde (MDA) in stroke mice. Moreover, genistein reversed the mitochondria dysfunction after ischemia, as evidenced by decreasing mitochondria ROS levels, preventing cytochrome C release to the cytoplasm and inhibiting caspase-3 activation. Western blotting showed ischemia activated the ROS-dependent nuclear factor-κB (NF-κB) signaling pathway, and genistein suppressed phosphorylation and activation of the NF-κB p65 subunit, as well as the phosphorylation and degradation of the inhibitor protein of κBα (IκBα). Our findings suggested that genistein has a neuroprotective effect in transient focal ischemia, which may involve regulation of mitochondria-dependent apoptosis pathways and suppression of ROS-induced NF-κB activation.

Apathy after stroke

What the hell is your doctor doing to correct this problem after your stroke? Any stroke protocols to correct this problem?
Maybe you need to read these and train your doctor.
The readable article here:

Apathy Explained: Why Some People Just Can’t Be Bothered

 “We know that in some cases people can become pathologically apathetic, for example after a stroke or with Alzheimer’s disease.
 Many such patients can be physically capable.

Yet they can become so demotivated they won’t be bothered to care for themselves, even though they’re not depressed.
Scans showed that the pre-motor cortex in the brains of apathetic people was consistently more active than in motivated people.

The research it is based upon here:

Individual Differences in Premotor Brain Systems Underlie Behavioral Apathy

This is fascinating since when I look at my dead brain area it looks like most of my premotor cortex on the right side is dead. And I have no apathy whatsoever. Is my left side premotor cortex taking up that task? So many questions and not one fucking person in the world to ask them of. 

Wednesday, November 25, 2015

Tech Tats: The Future of Wearables?

I could easily see this being used for stroke survivors, by adding a nano needle patch you should be able to monitor INR and cholesterol levels. A great stroke association would have hundreds of patents supplying money to be used in research. That's if we had any stroke leadership at all. Which we don't.
A forlorn girl sits at the bottom of a staircase in her household. An adult comes by with a small plastic case, opening it to reveal a rectangle sheet. The adult applies the sheet to the girl’s arm and holds a cloth over it. The cloth is pulled away and a small circuit board-like array with glowing green dots is stuck to the girl’s deltoid. The adult pulls out her smartphone, where the girl’s vitals are displayed.  
“Rather than going to the doctor once a year to get your physical, this Tech Tattoo can be something that you just put on your body once a year and it monitors everything that they would do in a physical and sends that to your doctor, and if there’s an issue, they could call you,” said Eric Schneider, a creative technologist with Chaotic Moon, the developer of Tech Tats, in a video.
“It can look at early signs of fever, your vital signs, heartrate, everything that it needs to look at to notify you that you’re getting sick, or your child is getting sick.”
According to Vice’s Motherboard, the tattoo uses electroconductive paint to transfer data from temperature sensors to an ATiny85 microcontroller.
While the focus is currently on the medical field, Schneider floats the idea of using the Tech Tat as a way to revolutionize the banking industry. Rather than carrying wallets around, credit cards and identification information can be stored right on one’s skin.
Speaking with TechCrunch, Chaotic Moon CEO Ben Lamm said, “The future of wearables is biowearables.” He added that the company is in talks with partners to bring Tech Tats to market.
Chaotic Moon is a software company based in Austin, Texas.

Memantine may not be covered through Medicare Part D

Memantine coverage
Memantine, which recently became available as a generic drug, may not be covered through Medicare Part D. If you or someone you know is taking memantine, check with your plan to inquire about coverage, or contact your State Health Insurance Program (SHIP) through Medicare and ask to speak to a counselor. You may also want to talk to your doctor regarding your options.

You probably don't have to worry about this because I'm 100% positive that the research from 2014 suggesting possible use for stroke has never been followed up on. I blame our fucking failures of stroke associations for that.

Study of the neuroprotective effects of memantine in patients with mild to moderate ischemic stroke

Our results reveal that memantine added to standard treatment of CTEE(cerebral thromboembolic event) could result in a remarkable decrease in the NIHSS confirming improvement of the neurological function of the patients. 

Early Magnesium Treatment After Aneurysmal Subarachnoid Hemorrhage

The failure could easily been because they were using invalid endpoints like the Rankin scale.

Individual Patient Data Meta-Analysis

  1. Walter M. van den Bergh, MD, PhD;
  2. on behalf of the writing groups of MASH-I, IMASH, MASH-II, MASH and FAST-MAG
+ Author Affiliations
  1. From the Department of Neurology and Neurosurgery, Rudolf Magnus Institute of Neuroscience (S.M.D.M., A.A., G.J.E.R.) and Julius Center for Health Sciences and Primary Care (A.A.), University Medical Center Utrecht, Utrecht, The Netherlands; Division of Neurosurgery, Department of Critical Care, Prince of Wales Hospital, The Chinese University of Hong Kong, Hong Kong, China (G.K.C.W., W.S.P.); Department of Critical Care, Royal North Shore Hospital, Sydney, Australia (C.M.B.); Department of Neurology (J.L.S.) and Departments of Emergency Medicine and Neurology (S.S.), Comprehensive Stroke Center, David Geffen School of Medicine at the University of California, Los Angeles; and Department of Critical Care, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands (W.M.v.d.B.).
  1. Correspondence to Walter M. van den Bergh, MD, PhD, Department of Critical Care, University Medical Center Groningen, University of Groningen, Room BA.49, PO Box 30001, 9700 RB Groningen, The Netherlands. E-mail


Background and Purpose—Delayed cerebral ischemia (DCI) is an important cause of poor outcome after aneurysmal subarachnoid hemorrhage (SAH). Trials of magnesium treatment starting &lt;4 days after symptom onset found no effect on poor outcome or DCI in SAH. Earlier installment of treatment might be more effective, but individual trials had not enough power for such a subanalysis. We performed an individual patient data meta-analysis to study whether magnesium is effective when given within different time frames within 24 hours after the SAH.
Methods—Patients were divided into categories according to the delay between symptom onset and start of the study medication: &lt;6, 6 to 12, 12 to 24, and &gt;24 hours. We calculated adjusted risk ratios with corresponding 95% confidence intervals for magnesium versus placebo treatment for poor outcome and DCI.
Results—We included 5 trials totaling 1981 patients; 83 patients started treatment &lt;6 hours. For poor outcome, the adjusted risk ratios of magnesium treatment for start &lt;6 hours were 1.44 (95% confidence interval, 0.83–2.51); for 6 to 12 hours 1.03 (0.65–1.63), for 12 to 24 hours 0.84 (0.65–1.09), and for &gt;24 hours 1.06 (0.87–1.31), and for DCI, &lt;6 hours 1.76 (0.68–4.58), for 6 to 12 hours 2.09 (0.99–4.39), for 12 to 24 hours 0.80 (0.56–1.16), and for &gt;24 hours 1.08 (0.88–1.32). The primary endpoint was poor clinical outcome (mrs 4-5) or death at 3-6 months, with a secondary endpoint of delayed cerebral ischemia (which was determined differently by each trial).
Conclusions—This meta-analysis suggests no beneficial effect of magnesium treatment on poor outcome or DCI when started early after SAH onset. Although the number of patients was small and a beneficial effect cannot be definitively excluded, we found no justification for a new trial with early magnesium treatment after SAH.