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:

Saturday, April 29, 2017

Researchers discover genes linked to resilience against brain pathologies

Not sure how I would test to see if I have these genes.
The pathologies (damage) in the brain that stroke, Alzheimer's disease and other neurological conditions cause in older adults only partially explain the memory loss, reduced reasoning ability and other cognitive impairments that result from these conditions. Little is known about why the effects of brain pathology vary between people who develop it.
Now researchers have discovered two genes, known as UNC5C and ENC1, that are associated with aging individuals having better memory and brain function than would be expected, given the amount of pathologies that accumulated in their brains. They reported their findings in an article published in the journal PLOS Medicine on April 24.
"Most of the cognitive loss that we experience in older age remains unexplained. Certain individuals are very resistant to the pathologies of the aging brain, while others may be particularly vulnerable," says study senior investigator David Bennett, MD, who directs the Rush Alzheimer's Disease Center.
These potentially damaging pathologies include the buildup of harmful proteins known as amyloid plaques and neurofibrillary tangles that occur in Alzheimer's disease; the protein deposits known as Lewy bodies that accompany Parkinson's disease and Lewy body dementia; and the death of massive amounts of brain cells caused by stroke.
Identifying genes that contribute to resistance to these and other brain pathologies could provide researchers with new targets for developing medications that would enhance the brains of aging adults to resist Alzheimer's disease and other neurological conditions, Bennett says.
Study used genetic analysis of 979 organ donors' brain tissue
The researchers drew on a vast trove of data, including genetic analyses, generated by two ongoing long-term studies of aging based at Rush University Medical Center, which includes study participants' donation of their brains for research after their death. These participants were tested annually to measure their cognitive function, allowing for a comparison of the decrease in cognitive function with the development of any pathology found when their brains were autopsied after their deaths.
Using this information for 979 participants, the researchers assessed how much each person's thinking ability withstood the development of memory loss despite the accumulation of brain pathology - in other words, how resilient they were to pathology. Then they conducted a complex, multiple step analysis "to identify segments of the human genome (i.e, genes) that help us to maintain cognitive function in the face of advancing age and disease," explains study senior investigator Philip De Jager, MD, PhD, professor of neurology at Columbia University Medical Center.
The innovative approach combined an analysis of the human genome - the complete set of genes in a person -- with an evaluation of the epigenome -- changes to DNA that helps determine which genes can be "read" so its protein is made. Epigenome in part reflects how our brain responds to life experiences and exposures to environmental factors.
The analysis identified UNC5C and ENC1 as being associated with cognitive resilience. In addition, the researchers found that TMEM106B -- a gene whose presence previously had been identified as possibly protecting against age-related frontotemporal lobar degeneration -- also may play a role in brain resilience.
"These genes should be studied further to expand our understanding of molecular mechanisms relevant to cognitive resilience that could be translated into prognostic and therapeutic tools for dementia prevention," the researchers write in the paper's summary.

dl-3-n-butylphthalide promotes neuroplasticity and motor recovery in stroke rats

Your doctor and hospital better get cracking on followup research in humans for this. With 10s of thousands of hospitals and doctors out there at least one should be able to solve this into a translational result.  But you know that will never occur, it hasn't occurred in the last 50 years it won't miraculously start occurring now.


dl-NBP promoted the behavioral performance after cerebral ischemia in rats.
dl-NBP improved the behavioral recovery possibly by increasing neurogenesis, axonal regeneration and synapse formation.
The axonal regeneration promoted by dl-NBP may be mediated through the Nogo-A/NgR and RhoA/ROCK pathway.


Backgrounds and aims

Racemic l-3-n-butylphthalide (dl-NBP), is able to achieve a functional recovery in animal models of cerebral ischemia, vascular dementia, and Alzheimer’s disease. In this study, we investigated the effect of dl-NBP on axonal growth, neurogenesis and behavioral performances in rats with cerebral ischemia.


Focal cerebral ischemia in rats was produced by intracerebral injection of endothelin-1. Starting from postoperative day 7, the experimental rats were administered 70 mg/kg dl-NBP by oral gavage for two weeks. Biotinylated dextran amine (BDA) was injected into the contralateral sensorimotor cortex on day 14 after ischemia to trace the sprouting of corticospinal tract (CST) fibers into the denervated cervical spinal cord. The expressions of Nogo-A, Nogo-R, Rho-A, and ROCK in the perilesional cortex, the expressions of BDA, PSD-95, and vGlut1 in the denervated spinal cord, 5-bromo-20-deoxyuridine (BrdU)/DCX-positive cells in the subventricular zone (SVZ) of the injured hemisphere were detected by immunofluorescence. The rats’ behavioral abilities were measured on postoperative days 30–32 in the beam-walking, cylinder and sticky label tests.


dl-NBP treatment significantly increased the number and length of crossing CST fibers, enhanced significantly the expression levels of synapse-associated proteins including PSD95 and VGlut-1 in the denervated cervical spinal cord, elevated the number of BrdU+/DCX+ cells in SVZ, and reduced markedly those of Rho-A+, ROCK+, Nogo-A+ and Nogo-R+ cells in perilesional cortex. In addition, dl-NBP improved the behavioral performance of the ischemic rats.


dl-NBP enhanced the behavioral recovery after cerebral ischemia in rats, possibly by increasing axonal growth and neurogenesis.


  • Axonal growth;
  • dl-NBP;
  • Neurogenesis;
  • Stroke
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Correspondence to: No.155, North Nanjing Street, Heping District, Shenyang 110001, Liaoning, China.

Does atrial fibrillation cause cognitive decline and dementia?

You'll have to have your doctor fix your AF and prevent your cognitive decline and dementia.
Or is the problem that fixing AF causes decline and dementia? Cause and effect analysis needed.

EP Europace
Dietzel J, et al.
Researchers assessed the impact of atrial fibrillation (AF) on cognitive function. They gathered and summarized the published literature data on the association between AF and cognitive decline and found evidence supporting the notion that AF independently confers risk for cognitive decline and dementia in general and for Alzheimer’s disease in particular. The possible mechanisms involved were: AF–related ischaemic stroke, white matter damage and systemic inflammation.

The effect of three different meditation exercises on hypertension: A network meta-analysis

I bet your doctor is choosing between 3-4 different blood pressure drugs and has no recommendation on this.  But then you should already be meditating to help your stroke recovery. 41 posts on meditation which your doctor has already told you about.
Evidence-based Complementary and Alternative Medicine
Yang H, et al.
An observational study was carried out to utilize the pairwise and network meta–analysis to assessment the impacts of various meditation exercises on the control of systolic blood pressure (SBP) and diastolic blood pressure (DBP). Qigong may be the optimal exercise way in lowering SBP and DBP of hypertensive patients, but a detailed long–term clinical research ought to be required later on.
  • They designed a network meta–analysis.
  • For this study, randomized controlled trials (RCTs) were retrieved from PubMed and Embase up to June 2016, which are published in English and reported on meditation exercise for hypertensive patients.
  • Risks of bias evaluation of the included studies were evaluated by Cochrane Collaboration Recommendations and network meta–analysis was performed by ADDIS.
  • Mean difference (MD) and its 95% confidence interval (CI) were utilized as the effect size.
  • In this study, total 19 RCTs were included.
  • The outcomes of pairwise comparisons showed that meditation exercise could majorly reduce the SBP and DBP, compared with other interventions (MD = –7.10, 95% CI: –10.82 to –3.39; MD = –4.02, 95% CI: –6.12 to –1.92).
  • With good consistence and convergence, network meta–analysis demonstrated that there were no important differences between meditation and other interventions on SBP.
  • For DBP, Qigong was significantly lower than “no intervention” (MD = –11.73, 95% CI: –19.85 to –3.69).

Does supplementation with omega-3 PUFAs add to the prevention of cardiovascular disease?

But all these other benefits. But then your doctor has already told you all you need to know on this.

Research shows fish oil component helps damaged brain and retina cells survive


Fish Oil Injection to Stroke Victims: Remedy for Brain Damage  Feb. 2013


Aspirin plus fish oil for a hyperacute treatment.  Feb. 2012


Our findings suggest that consuming DHA regularly protects the brain against fructose's harmful effects


Fish consumption and omega-3 fatty acid supplementation for prevention or treatment of cognitive decline, dementia or Alzheimer's disease in older adults any news?


Best Supplement To Improve Memory In Healthy People - Omega-3s
Current Cardiology Reports
Rizos EC, et al. – Researchers conducted this study to re–assess the impact of omega–3 supplements on all–cause and cardiovascular mortality, myocardial infarction, and stroke. They searched for and analyzed data from the relevant randomized controlled trials to derive the conclusion that the proposed benefits of omega–3 supplementation in cardiovascular disease were not consistent but uncertain.


  • Researchers analyzed data from 21 randomized controlled trials assessing the impact of omega-3 supplementation on mortality and cardiovascular-related outcomes.


  • From these studies, as well as from the relevant meta-analyses, they found that omega-3 supplements did not exert a consistent benefit for cardiovascular protection.

Drinking coffee basically keeps you alive

I think I have most of the research backing these up, if you are interested ask your doctor.  I don't recall the hospital even serving coffee
Quite the eye catching headline there. I think have have written about most of these, ask your doctor for details.

Originally Published By:

Three strong cups of coffee a day slashes the risk of prostate cancer by half, a study revealed this week.
And that’s only one of its benefits.

Prevents high cholesterol

Coffee helps prevent clogging of the arteries, according to a study in the British Medical Journal.
And a US team found women drinking a cup a day can slash the risk of stroke by up to 25 percent.

Reduces risk of heart disease

Three to four cups daily cuts the risk of heart disease, a Portuguese study found.
In the US, Harvard researchers found that low consumption of coffee and deaths from heart-related illnesses are linked.

Protects the brain

Coffee makes you feel more alert – although scientists are unsure how it also helps maintain brain function.
And Dutch research shows coffee slashes the chance of developing Alzheimer’s by 20 percent.

Reduces risk of dying

Researchers at Harvard found three to five cups of coffee a day could stop you heading to an early grave.
The study also found it reduces the risk of developing neurological diseases such as Parkinson’s.

Helps you heal

Coffee is shown to speed up the healing process, helping faster recovery from operations and wounds.
A German study in 2012 found drinking 3 ounces three times per day helped patients recover from bowel operations faster.

Clean teeth

Coffee breath could actually be a sign of clean teeth.
Scientists at Rio de Janeiro’s Federal University found that coffee breaks down bacteria which causes plaque.
Drinking it could slow down or even prevent tooth decay.

Lowers risk of diabetes

Having more than one cup daily cuts the risk of Type 2 diabetes by 11 percent, researchers from Singapore found.
A US study found three to five cups a day could also help diabetics stabilize their blood sugars.

Friday, April 28, 2017

Lifestyle Program May Slow Cognitive Decline

I bet this could adapted for stroke survivors. It will never occur, we have such absolute stupidity in stroke with NO STRATEGY AND NO LEADERSHIP.

At-risk seniors seem to benefit from nutritional guidance, vigorous exercise

  • by
    Contributing Writer, MedPage Today

Action Points

  • Note that this study was published as an abstract and presented at a conference. These data and conclusions should be considered to be preliminary until published in a peer-reviewed journal.
BOSTON -- A program that provides elderly people at risk for dementia with dietary guidance, exercise, cognitive training, and vascular risk monitoring could prevent cognitive decline, researchers said here.
Prevention has been highlighted "as a key element in managing dementia, said Miia Kivipelto, PhD, of the Center for Alzheimer Research and Aging Research Center, Karolinska Insitutet in Stockholm in a presentation at the American Academy of Neurology annual meeting.
"At the same time it is increasingly clear that it is very difficult to find new drug treatments for Alzheimer's disease and dementia," she noted.
While there has been evidence in observational studies that modifiable vascular and lifestyle-related risk factors are associated with dementia risk, what has been lacking has been evidence from randomized control trials showing that modifying these risk factors can prevent cognitive decline, she noted.
The Finnish Geriatric Intervention Study to Prevent Cognitive Impairment and Disability (FINGER) study is a proof-of-concept randomized control trial designed to assess a "multidomain" approach to preventing cognitive decline in at-risk elderly persons. The results of the study were originally published in the Lancet.
In this trial conducted from 2009-2011, researchers enrolled individuals between the ages of 60-77, with 631 randomly assigned to the multidomain intervention group, and 629 to the control group. Inclusion criteria include CAIDE (Cardiovascular Risk Factors, Aging, and Incidence of Dementia) Dementia Risk Scores of at least 6 points, and cognition at mean level or slightly lower than expected for age.
Individuals in the intervention group were given nutrition guidance, put on increasingly vigorous exercise regimens, and provided with cognitive training. Their metabolic and vascular risk factors were also monitored and managed. The control group was provided with general health advice.
"As expected, both groups improved over the 2 years, but the intervention group improved much more," Kivipelto said.
The primary outcome was cognitive change as measured through a comprehensive neuropsychological test battery Z score.
The impact of the intervention on global cognition was significantly higher, said Kivipelto, with the intervention group showing a 25% greater improvement over baseline scores compared with the control group.
That pattern also held for outcomes such as executive functioning (83% improvement), processing speed (150%), and complex memory tasks (40%).
"We also saw that the control group had a 30% increased risk of cognitive decline [versus the intervention group] over the 2 years," she said.
Kivipelto added that new data from the trial also indicated that the intervention was beneficial regardless of sociodemographic factors, baseline cognition, or cardiovascular risk factors. "This indicates that the selection of the target group was successful and that this type of intervention may be implemented in a wider population."
The intervention also had positive effects on secondary outcomes such as activities of daily life (ADL) function, mobility, and quality of life. For example, the intervention group had a 30% lower risk of a decline in ADL function versus the control group.
While adverse events occurred in 46 (7%) of the people in the intervention group, compared with six (1%) in the control group, "there were no serious adverse events," Kivipelto said, adding that most adverse events involved slight muscular pain related to exercise.
As for future research in this area, "I think it will be very important in the future to have even larger multidomain, multinational studies, with tailored interventions, and pragmatic prevention programs," Kivipelto said.
Kivipelto disclosed no relevant relationships with industry.

“Good Outcome” Isn’t Good Enough - post-stroke

Using the Rankin scale as a measurement device for stroke disability is incredibly stupid. It has nothing objective in it at all except for 6 - death.

Cognitive Impairment, Depressive Symptoms, and Social Restrictions in Physically Recovered Stroke Patients

Arunima Kapoor, Krista L. Lanctôt, Mark Bayley, Alex Kiss, Nathan Herrmann, Brian J. Murray, Richard H. Swartz


Background and Purpose—Functional outcome after stroke is often only evaluated using the modified Rankin Scale, which primarily assesses activities of daily living. Stroke patients may experience difficulties with social reintegration and mental functions, feel isolated, and experience poor quality of life, even after physical recovery is complete. Functional assessments based solely on activity limitations may not be able to capture the full range of problems experienced by stroke survivors.
Methods—Telephone interviews were conducted 2 to 3 years poststroke to assess outcome on multiple levels of functioning as stated in the WHO International Classification of Functioning: body function (Montreal Cognitive Assessment and Patient Health Questionnaire-2), activity (modified Rankin Scale), and participation (Reintegration to Normal Living Index).
Results—Ninety-six (68%) patients had a favorable functional outcome (modified Rankin Scale <2). Of these, 79, 91, and 93 patients completed the Montreal Cognitive Assessment, Reintegration to Normal Living Index, and Patient Health Questionnaire-2, respectively. Forty-three (54%) patients were cognitively impaired, 47 (52%) had restrictions in reintegration, and 30 (32%) endorsed symptoms of depression. There was no difference in Montreal Cognitive Assessment or Patient Health Questionnaire-2 scores between those who had activity limitations and those who had not.
Conclusions—More than half of stroke patients with excellent functional recovery measured by the modified Rankin Scale continue to have cognitive impairment and participation restrictions, and one third of patients continue to have depression 2 to 3 years later. Current definitions of good functional outcome used in the majority of stroke acute trials focus on activity limitations, but greater attention to multiple levels of recovery is required.

Stroke symptoms go unnoticed in young adults

Because the objective diagnosis of young adult strokes is so bad you better have the complete classic symptoms(drooping face, slurred speech, one-sided paralysis and lack of sensation). And still hope your doctor doesn't consider you drugged.

Pediatric Stroke Often Misdiagnosed, Treatment Delayed


Doctors tell boy, 15, he had a migraine after rugby tackle - but he was actually suffering a paralyzing stroke which nearly killed him


Factors Associated With Misdiagnosis of Acute Stroke in Young Adults


Amy on her 36 hour wait for a diagnosis.

And the blame the victim here:

  Stroke symptoms go unnoticed in young adults

Up to one in ten new strokes occur in people under 45. And the number of strokes in people aged 20 to 64 is increasing, up by 25 per cent from 1990 to 2010 worldwide, according to the Stroke Association.
Increased prevalence of high blood pressure and diabetes as well as more sedentary lifestyles may be among the factors involved, but in up to half the cases in younger people, the cause is unknown.
Although stroke is mostly associated with the elderly, 2015 UK data reported by the Stroke Association shows that 26 per cent occur in the under-65s and around one in a hundred and fifty in the under-20s. According to the South London Cardiac and Stroke Network, up to 12 per cent of first strokes occur in patients under 45.
About a quarter of all strokes in the UK affect people of working age, according to NHS figures reported by the Stroke Association. National data from the United States, in the Journal of the American Heart Association, shows that over the decade up to 2010, hospitalisation rates for stroke increased by 43.8 per cent in the 25 to 44 age group.

Why the rise?

Just why it is increasing is unclear, although there are many theories. A study reported by the Stroke Association found that 62 per cent of young adults were actively engaged in smoking, alcohol excess or illegal drug use at the time of the stroke.
Dr Anthony Pereira, consultant neurologist at St George’s Hospital in London, and co-author of the Oxford Handbook of Stroke Medicine, says: “There is no clear-cut reason for the rising numbers. The Stroke Association has launched a campaign to raise awareness of warning signs and that may have led to more young people presenting.
“Improved imaging also means that we can detect more strokes, which again may have led to an apparent increase because strokes tend to be milder in young people and not as easily spotted. Younger people now lead more sedentary lifestyles, which could be a factor too.
There are many powerful myths about stroke, for example that it only affects older people
“The prevalence of diabetes and high blood pressure is increasing. Hypertension is the major risk factor for stroke and younger people may be less aware of their blood pressure, but they do need to understand that high blood pressure is very important and needs to be treated early. We have seen people presenting with eye-wateringly high blood pressure.”
Stroke in younger people may also have a different profile. Bigger strokes are more likely to be haemorrhagic or bleeding strokes, rather than the more common ischaemic strokes, where a bloodclot blocks the flow of blood to the brain.
In the under-45s, up to half of strokes are ischaemic compared with 85 per cent in older patients, according to a 2010 report by the South London Cardiac and Stroke Network. That may be because younger adults have a better collateral blood supply that is more able to cope.


ANNUAL STROKE-RELATED DEATHS IN THE UKOne of the challenges is that stroke is seen as a disease of older people and may not be considered as a possibility in younger people, which can lead to delays in diagnosis and treatment.
“Stroke is often not recognised as a possible diagnosis in young adults,’’ says Dr Richard Perry, consultant neurologist and hyperacute stroke research lead at University College London Hospitals NHS Foundation Trust.
“Patients and many doctors do not think of stroke when a young adult presents with less obvious symptoms, such as sudden unsteadiness. While major symptoms such as loss of movement all down one side of the body will usually be picked up, less specific symptoms can be overlooked in younger people.
“That is a problem because rapid diagnosis is essential for clot-busting drugs to be effective. The London Ambulance Service use a protocol called FAST – Face, Arms, Speech, Time – where crews take notice of these symptoms and ignore age. We would rather screen people who fulfil these criteria and have not had a stroke, rather than miss those who have.”
Alexis Wieroniey, Stroke Association deputy director of policy and influencing, says that increasing recognition of stroke as a possible diagnosis is important. She says: “There are many powerful myths about stroke, for example that it only affects older people, and these stop people from taking action to prevent stroke. The truth is a quarter of strokes happen to people of working age and we all need to change the way we think about this devastating condition.”
There is a financial incentive to detecting stroke early in young people too, because they may survive major strokes for many more years than older patients, incurring greater costs.

10 Stroke Risk Factors from the American Stroke Association

Great conscience laundering but does nothing for the millions of stroke survivors out there. More awareness only.NO solutions.

Guargantuan Fucking Whoopee.

Researchers call for better surveillance systems to track stroke incidence over time

And why would we need this? Everything in stroke is going perfectly. There are no problems being reported. F.A.S.T. and prevention and awareness efforts are all that is needed . Didn't you get the message from last World Stroke Day that stroke is treatable?

 - Tim Casey
Tim Casey, Executive Editor

During the past several years, stroke mortality rates have declined thanks to hypertension control, quality improvement programs, evidence-based care and increased medication use.
At the same time, younger adults are increasingly getting hospitalized for strokes, according to a recent database analysis.
The researchers, who published their findings in JAMA Neurology on April 10, found that acute ischemic stroke hospitalizations rates increased 30 percent among women and 41.5 percent among men who were between 35 and 44 years old between 2003 and 2012. In 2012, there were nearly 30,000 more stroke hospitalizations than there were in 2003.
Still, James F. Burke, MD, MS and Lesli E. Skolarus, MD, MS, wrote in an accompanying editorial that the increases might not be as eye-opening as they appear at first glance.
“If these findings represent a true epidemiologic trend, understanding the reasons underlying this trend and seeking to reverse it should be a leading priority of the stroke community,” they wrote. “However, it is not yet clear whether such urgent action is needed.”
Burke and Skolarus noted that population growth alone accounts for approximately 15,000 additional strokes per year in the younger age category. They also mentioned that the researchers gathered data from the National Inpatient Sample (NIS), a publicly available database of hospital inpatient stays in the U.S. Thus, they speculated that the accuracy of counting strokes could be questioned because of changes in stroke terminology and care from 2003 to 2012.
The researchers also found that younger adults had an increase in vascular risk factors such as hypertension, lipid disorders tobacco use and obesity, although Burke and Skolarus wrote that the increase could be due in part to more accurate coding.
“If, ultimately, stroke in the young is truly increasing and many of these strokes were preventable, it would represent a massive failure not only of our health care system, but also our stroke surveillance systems for failing to clearly detect the trend and enable it to be acted on,” they wrote. “Developing better surveillance systems, then, should be a priority of the stroke research community. A number of potential solutions exist: collecting more widespread epidemiologic data, harmonizing and building cooperation between existing epidemiological studies, or developing more reliable administrative- or electronic medical record–based surveillance systems. As the richest health care system on the planet, the answer to the question of whether stroke in the young is increasing should never be ‘Maybe.’ The authors of the present study should be commended for their effort to help resolve this uncertainty.”

Nose2Brain – Better Therapy for Multiple Sclerosis

An efficient delivery method to the brain whenever we get drugs that need to be delivered there.
Medically active substances are normally distributed via the blood – either directly by injection into the bloodstream or indirectly, for example through the digestive tract after oral administration. In many diseases, however – for example of the central nervous system – it is of decisive importance to transport the active substance as efficiently as possible to the required target site. An example of this is the treatment of multiple sclerosis, where the pharmaceutical agents have to produce their effect above all in the central nervous system. However, this is especially difficult to achieve in the usual way via the blood due to special protective mechanisms such as the blood-brain barrier.
Through the nose direct into the brain
Within the scope of the EU-funded “N2B patch” cooperative project, Fraunhofer IGB is therefore participating in the development of a medical form of therapy that delivers the drug via the Regio olfactoria. The aim of this alternative approach is to enable an active substance to circumvent the path through the bloodstream and to reach the brain directly. Here the brain, together with the surrounding liquid, is only separated from the nasal cavity by the ethmoid bone and some cell layers. The active agent can easily penetrate this barrier and reach the brain directly taking a short route. The therapeutic system will consist of the active agent itself, of a formulation containing the active agent, a hydrogel as carrier material for the formulation, and a suitable applicator for inserting the patch in the nose. The active agent is a biomolecule that stimulates the regeneration of nerve cells.
In the project the scientists at Fraunhofer IGB are concentrating on the formulation of the particles containing the active agent, and on inserting these particles into the gel. The project consortium is developing a special applicator to introduce the gel into the nose. The device is a combination of a standard endoscope and a special mixing system. This system is necessary as the target site is difficult to reach and an already solidified gel could not be deposited in the correct place. The liquid precursors of the gel therefore have to be transported separately to the olfactory epithelium inside the nose. There the various components combine to form a gel with the required consistency, so that the patch remains securely in place.
As the olfactory epithelium is difficult to reach, the gel patch should be applied by a doctor, not by the patients themselves. The active agent will then be released over an extended period of time, so there is then no need to remove the patch again. A new one is simply inserted in the case of long-term treatment.
EU funds Nose2Brain project for four years
The N2B patch project is supported financially by the EU within the scope of the tender procedure “Biomaterials for diagnosis and treatment of demyelination disorders of the central nervous system”. A total of eleven partners from research and industry are participating in the project, which is scheduled to last four years and will be completed at the end of 2020. The special focus of the participating researchers is on the treatment of multiple sclerosis; however, they also hope to develop other fields of application for the N2B platform.

Reducing the metabolic cost of walking with an ankle exoskeleton: interaction between actuation timing and power

Stroke use and clinical testing needs a followup on this. Assisting dorsiflexion and plantatflexion(push off) would be a massive win for those survivors with drop foot. 11 years later and I still have no push off.
Contributed equally
Journal of NeuroEngineering and Rehabilitation201714:35
DOI: 10.1186/s12984-017-0235-0
Received: 10 September 2016
Accepted: 17 March 2017
Published: 27 April 2017



Powered ankle-foot exoskeletons can reduce the metabolic cost of human walking to below normal levels, but optimal assistance properties remain unclear. The purpose of this study was to test the effects of different assistance timing and power characteristics in an experiment with a tethered ankle-foot exoskeleton.


Ten healthy female subjects walked on a treadmill with bilateral ankle-foot exoskeletons in 10 different assistance conditions. Artificial pneumatic muscles assisted plantarflexion during ankle push-off using one of four actuation onset timings (36, 42, 48 and 54% of the stride) and three power levels (average positive exoskeleton power over a stride, summed for both legs, of 0.2, 0.4 and 0.5 W∙kg−1). We compared metabolic rate, kinematics and electromyography (EMG) between conditions.


Optimal assistance was achieved with an onset of 42% stride and average power of 0.4 W∙kg−1, leading to 21% reduction in metabolic cost compared to walking with the exoskeleton deactivated and 12% reduction compared to normal walking without the exoskeleton. With suboptimal timing or power, the exoskeleton still reduced metabolic cost, but substantially less so. The relationship between timing, power and metabolic rate was well-characterized by a two-dimensional quadratic function. The assistive mechanisms leading to these improvements included reducing muscular activity in the ankle plantarflexors and assisting leg swing initiation.


These results emphasize the importance of optimizing exoskeleton actuation properties when assisting or augmenting human locomotion. Our optimal assistance onset timing and average power levels could be used for other exoskeletons to improve assistance and resulting benefits.


Human locomotion Augmentation Lower-limb exoskeletons Metabolic cost Optimal assistance


Walking is the most frequent means of human locomotion [1]. While humans use many strategies to reduce energy expenditure [2], walking still requires a considerable amount of metabolic energy, sometimes referred to as the ‘metabolic cost’ of walking. Assisting the ankle joint with an exoskeleton can reduce the metabolic cost of walking to below the cost of normal walking [3, 4, 5, 6]. This shows that it is possible to reduce metabolic cost through robotic assistance.
Reductions in the metabolic cost of walking with ankle-foot exoskeletons result from two competing factors. A benefit can be derived from the exoskeleton when it acts to assist gait, expressed as the difference between powered exoskeleton1 walking and walking in zero-work mode1. However, wearing the exoskeleton in zero-work mode typically results in a metabolic penalty, expressed as the difference between normal walking1 without an exoskeleton and walking in zero-work mode. Some full-body exoskeletons have resulted in large metabolic penalties (e.g. [7]) while lightweight ankle-foot exoskeletons have resulted in penalties of less than 3% for active autonomous1 exoskeletons [4] and even close to zero for passive autonomous1 exoskeletons [5]. Reducing the penalty of wearing an exoskeleton in zero-work mode is mainly a design challenge, while increasing the difference between the zero-work condition and powered exoskeleton conditions is mainly a biomechanics challenge.
In order to solve the latter human-exoskeleton interaction challenge, optimal assistance properties (e.g. actuation timing, assistance magnitude, etc.) are crucial to further reduce the metabolic energy cost of walking. Malcolm et al. [3] showed that the timing of exoskeleton actuation onset (referred to as actuation timing) is an important exoskeleton property that influences the metabolic cost of walking with active exoskeletons. They found a convex landscape in metabolic cost versus actuation timing with an optimum around 40% of the stride. Studies that have found the highest reductions in metabolic energy cost have also used an actuation timing around 40% of the stride [4, 6].
Of course, actuation timing is not the only determinant of metabolic cost when walking with ankle-exoskeleton assistance. Assistance magnitude also seems to have a strong effect [8, 9]. The average positive mechanical exoskeleton power per stride summed for both ankles (referred to here as exoskeleton power) can be as high as 0.38 W∙kg−1 resulting in reductions in net metabolic cost of between 10 and 22% for powered exoskeleton conditions compared to zero-work conditions [3, 4, 6, 8, 10, 11, 12]. However, comparing these studies does not result in a clear relationship between exoskeleton power magnitude and metabolic cost, likely because many factors differ between studies (e.g. design, exoskeleton mass, actuation profile, etc.), confounding comparisons. The simplest walking model [13] would suggest that increasing exoskeleton power will reduce the mechanical energy requirements for walking until subjects walk with zero metabolic cost. Indeed, a recent study, in which both ankle and hip joints were assisted with a soft exo-suit [8] indicated that metabolic energy cost reduces linearly with increasing exoskeleton assistance magnitude, similar to some findings with active prostheses [9]. On the other hand, a study on unilateral exoskeleton assistance suggested an exponential relationship between device power and metabolic cost [14]. Experiments and simulation studies with exoskeletons have similarly suggested that under some conditions “more is not always better” [5, 15, 16]. Interpretations have been made more difficult by the limited range of attainable levels of exoskeleton power, which has often been between 50 and 80% of biological ankle power [4, 10, 11].
In order to study if and when the reduction in the metabolic cost of walking begins to level-off with increasing exoskeleton power during bilateral exoskeleton assistance, it seems necessary to deliver more power than in current studies. To identify the influence of exoskeleton power magnitude on the metabolic cost of walking, as well as the interaction with actuation timing, there is a need for a parametric study of actuation timing and exoskeleton power over a larger range. A study of both actuation characteristics is also expected to contribute to an improved understanding of the assistive mechanisms of ankle-foot exoskeletons. Several studies have indicated that other joints besides the ankle joint are involved in the reduction in metabolic cost experienced when using an ankle-foot exoskeleton [3, 4, 5, 8, 12, 17, 18] but the exact mechanisms are unclear. Exploring different assistance parameters over a broad range would help to identify the relationship between biomechanical changes and the resulting changes in metabolic cost.
The overall goal of this study was to characterize the relationship between ankle exoskeleton power, actuation timing, and metabolic cost during walking over a broad range. We used a tethered and powered plantarflexion-assisting exoskeleton to vary actuation onset timing and average exoskeleton power independently and over a broad range and studied the influence of these characteristics on the metabolic energy cost of walking. We expected a second-order effect of actuation timing on metabolic energy cost [3] and explored several candidate relationships between exoskeleton power and metabolic energy cost to evaluate the interaction between timing, power and metabolic cost. A secondary goal was to use the best relationship to define optimal assistance parameters. Finally, we analyzed muscle activation, exoskeleton kinetics and walking kinematics that describe the neuromechanical interaction between the exoskeleton and the human, with the goal of explaining the reduction in metabolic cost and improving our understanding of human-exoskeleton interaction.

More at link.

Cannabis use and outcomes in patients with aneurysmal subarachnoid hemorrhage

Another biased report. It is far more likely than these people are self treating themselves with marijuana and that use has zero to do with the progression or cause of the disease. But Big Pharma doesn't want an easily available and grown intervention to decrease their profits. So the demonization continues.

My 13 reasons for marijuana use post-stroke.  

But don't listen to me, I have absolutely no medical training. And since I'm stroke-addled my reasoning skills are non-existent. I will get some after my next stroke even if I have to travel to  one of these states or Uruguay or Netherlands or North Korea and soon Canada.

This animated map shows where marijuana is legal in the US
Behrouz R, et al.
The objective was to evaluate the relationship between cannabis use and outcomes in patients with aneurysmal subarachnoid hemorrhage (aSAH). The authors offer preliminary data that CB+ is independently associated with delayed cerebral ischemia and possibly poor outcome in patients with aSAH. The findings add to the growing evidence on the association of cannabis with cerebrovascular risk.


  • Records of consecutive patients admitted with aSAH between 2010 and 2015 were reviewed.
  • Clinical features and outcomes of aSAH patients with negative urine drug screen and cannabinoids-positive (CB+) were compared.
  • Regression analyses were used to assess for associations.


  • The study group consisted of 108 patients; 25.9% with CB+.
  • Delayed cerebral ischemia was diagnosed in 50% of CB+ and 23.8% of urine drug screen negative patients (P=0.01).
  • CB+ was independently associated with development of delayed cerebral ischemia (odds ratio, 2.68; 95% confidence interval, 1.03-6.99; P=0.01).
  • A significantly higher number of CB+ than urine drug screen negative patients had poor outcome (35.7% versus 13.8%; P=0.01).
  • In univariate analysis, CB+ was associated with the composite end point of hospital mortality/severe disability (odds ratio, 2.93; 95% confidence interval, 1.07-8.01; P=0.04).
  • However, after adjusting for other predictors, this effect was no longer significant.

Thursday, April 27, 2017

Regenerative Angiogenesis Quality Over Quantity

We need this. What is your doctor doing to create angiogenesis in your brain?
Matthew J. Durand, Karima Ait-Aissa, David D. Gutterman
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Angiogenesis can broadly be defined as the growth of new capillaries and blood vessels. A complex set of multiphasic signaling pathways regulate angiogenic blood vessel growth,1,2 and these pathways have been the target for both pro- and antiangiogenic therapies. Angiogenesis is a fundamental physiological process that is required for fetal development, wound healing, and tissue repair after ischemic damage. For these reasons, promoting proangiogenic pathways has therapeutic potential to combat diseases where tissue blood flow is compromised, such as peripheral artery disease, ischemic heart disease, or after ischemic stroke. Thus, quantitative methods to assess the degree of angiogenic growth are critical.
Article, see p 1453
Typically, blood vessel density and the degree of angiogenic growth are quantified histologically by counting the number of capillaries observed in a defined cross section of tissue. When angiogenesis occurs, the ratio of capillaries per tissue surface area increases. Functional measures of angiogenesis include measuring perfusion to the tissue involved, and it is typically expected that these parameters (vascular density and perfusion) change in parallel. However, this is not always the case.1 In fact, injured tissue may demonstrate both an increase in capillary density and an increase in blood flow but still have underperfused areas. Such a discrepancy could be because of improper vasoregulation of new vessels, or creation of arteriovenous anastomoses that maintain overall tissue flow, …
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Parkinson’s Relief May Come From a 150-Year-Old Drug

You may need this, ask your doctor for Parkinson prevention protocols.

Parkinson’s Disease May Have Link to Stroke

Parkinson’s Relief May Come From a 150-Year-Old Drug 

Thu, 04/27/2017 - 3:14pm
by Kenny Walter - Digital Reporter -

Patient-Reported Outcomes and the Elephant in the Conference Room

Did your hospital do anything with your patient reported outcome of your stroke rehab? YOU MEAN YOU DIDN'T HAVE ANYONE ASKING YOU ABOUT HOW WELL YOUR STROKE PROTOCOLS GOT YOU TO 100% RECOVERY?
Patient-reported outcomes (PROs), defined as outcomes reported by patients without filtering or interpretation by others, are an important part of patient-centered research and care. The applications of PROs are varied and complex. They sit like an elephant in a room full of people, each of whom is touching his or her small part. No person can see beyond what is directly in front of him or her to the full picture.
At FasterCures, we see great potential in more effectively using PROs to advance the science of patient input. This year we are launching a new project under our Patients Count program to help provide a wider angle view of PROs and to reveal the big picture of their potential. The time is right for this approach.
While many agree in theory that PROs used in research and clinical care should be based on what patients report as being most important to their disease management, health and well-being, this has often not been adequately considered. For example, a PRO might capture whether a patient with arthritis can dress him or herself. In the patient’s experience, however, the time it takes to dress is a better measure of how well he or she is doing. This misalignment of measures hurts efforts to create patient-centered research and care.
Making PROs themselves truly patient-centered is one element of the challenge ahead. Another challenge is aligning various stakeholders’ interest in, and use of, PROs. As a starting point, we have identified the relevant parties and their interest or stake in PROs.
Patients and caregivers have the most “skin in the game.” There is no substitute for patients being able to base treatment decisions on outcomes that a) matter to them, b) are gathered from large numbers of patients like them and c) are specific to the treatment options available. Patients are eager for information collected from them to be used to improve and accelerate patient-centered discovery, design, development and delivery of medical products.
Drug and Device Companies
Companies want the PRO data they collect to be used in regulatory decision-making and the information they communicate to health-care providers, payers and patients about their medical products. Companies include PROs in clinical trials to help understand efficacy, safety, adverse events, tolerability and other potential benefits and harms. In spite of this investment, a recent study documented a steady decline in PRO data on labels for new drug applications. While companies are collecting PROs, the information about a product’s effect on these measures is not routinely making it to patients and providers for care decision-making.
Hospital systems and provider groups use PROs and other tools to understand clinical care outcomes, or the way particular care approaches affect patient health and health-care utilization at the population level. As the health-care system as a whole moves toward value-based health care, there is a greater focus on engaging patients and measuring clinical outcomes that matter to them, rather than simply billing for services rendered.
Physicians and other health-care providers frequently use PROs to assess how well individual patients feel or function as a basis for shared decision-making about care options. And they use PROs to monitor how well an individual is doing on his or her course of therapy.
There is growing recognition that PROs can be useful in establishing the value and comparative effectiveness of medical interventions, both of which are important factors for payers determining medical coverage and reimbursement policies.
Researchers apply their expertise to develop PROs that capture the domains of interest and meet scientific standards sufficient to be used in decision-making.
The Food and Drug Administration (FDA) encourages sponsors to use PROs to help demonstrate the safety and efficacy of drugs and medical devices, both in clinical trials and after products are made available to patients. In spite of numerous efforts, including a 2009 guidance outlining a process to validate PROs, many companies feel the expected standards are too rigid and the process too lengthy and unpredictable. There is great interest in resetting expectations, and FDA has committed to revisiting its guidance by 2021.
Patient Organizations
Many patient organizations are contributing to efforts to create patient-centered PROs specific to their condition. They also assist in collecting PROs through patient registries and other means that can describe the natural history of the condition, inform research and regulatory decisions, and improve patient care and access.
With so many parties taking a stake in PRO development and utilization, and each from a different vantage point, it’s easy to understand why this particular elephant is tough to get in full view. Our objective at FasterCures will be to invite stakeholders to step back, take a broader look and approach the challenges from a more holistic perspective. From there we hope to identify opportunities to streamline the path to making PROs a stronger foundation for the science of patient input.