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:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal.

Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.
My back ground story is here:

Wednesday, June 19, 2019

The National Stroke Programme for England: How to achieve world-class stroke care

Wrong, wrong, wrong. Stroke survivors don't want care, they want recovery. It is quite simple. You write your own stroke strategy based upon solving all these problems in stroke. You want results not processes, or guidelines or standards of care.  It is your responsibility to educate these people.  Hand that strategy to your government and get it implemented. Waiting for the government to do something is fucking useless. You are on your own, you have solve it yourself. 

The National Stroke Programme for England: How to achieve world-class stroke care

Juliet Bouverie, Chief Executive of the Stroke Association, tells us how the NHS Long Term Plan and National Stroke Programme have the potential to transform stroke services across England in the next five years

This is an exciting time to be working in stroke. We know how to detect and manage the two main risk factors for stroke, there are real advances in stroke treatment and stroke research is started to indicate some exciting breakthroughs. In England, there is a clear recognition now, from those in government and across the stroke community, that we must work together to tackle one of the biggest health challenges of our time. The NHS Long Term Plan and National Stroke Programme are vital to achieving this. (Not if 100% recovery is not your goal)

NHS Long Term Plan and the National Stroke Programme

Stroke affects 1.2 million people across the UK and remains the fourth biggest killer and the largest cause of adult disability. Every five minutes, stroke destroys lives. And it turns the lives of carers and families upside down. This is why it is reassuring to see stroke included as a new clinical priority in the NHS Long Term Plan.
As well as saving half a million lives through improved CVD prevention, NHS England’s plan promises to increase access to thrombolysis and thrombectomy treatments, to overhaul the stroke workforce and to transform rehabilitation models post-stroke. This is a big opportunity for us all. Collectively achieving these ambitions would help hundreds of thousands more people each year to rebuild their lives after stroke.
In partnership with NHS England and others, the Stroke Association has developed the National Stroke Programme for England, supporting the Long Term Plan’s aims. As co-chair of the Stroke Programme Delivery Board, I’m encouraged to see work progressing across the five main priority areas – preventing strokes, redesigning acute stroke services, improving rehabilitation and ongoing care, modernising the workforce and strengthening date and research.

The vehicle for change: hyper-acute stroke units

Across England, we need to look at the very basic structure of stroke services. Do local stroke pathways actually make sense, provide quality care for all and integrate acute and post-acute services?
Here, the hyper-acute stroke unit (HASU) model of stroke services, taking patients to hyper-acute centres of excellence rather than the nearest hospital A&E department, is vital. Robust evidence shows us that this model is effective at saving lives, reducing the chance of disability and shortening the time spent in hospitals. This is why the Stroke Association fully supports efforts to reconfigure stroke services into HASUs.
In London and Manchester, reconfiguring services into the HASU model has saved an average of 100 and 70 extra lives per year respectively and Northumbria has seen significantly improved patient outcomes. Evidence shows that stroke patients treated in HASUs are more likely to survive and recover more quickly because these units are fully staffed and equipped and set up to deliver specialist and effective care 24/7. This also helps to address the significant workforce shortages and challenges in stroke by concentrating specialist stroke skills and expertise under one roof.
Yet across the country, public and political opposition often stands in the way of reconfiguring stroke services into HASU models, leading to patchy progress.
Through the National Stroke Programme, work will also soon start to develop Integrated Stroke Delivery Networks (ISDNs) in all areas of England, bringing people and organisations together to create the best stroke pathway possible for local populations. Creating HASUs should be a top priority. It is proven to improve outcomes and we simply cannot afford to delay a process that will save lives.

Accessing game-changing treatments

Currently, only 10% of eligible patients have access to mechanical thrombectomy, a game-changing clot-retrieval treatment that reduces the severity of the disability that a stroke can cause. In some cases, thrombectomy also saves lives.
We want all eligible patients to access this transformative treatment as soon as possible, regardless of where they live. Again, we will only make real progress here once we get the basics right – properly and efficiently organised stroke services in each region delivered round the clock and enough stroke specialists trained up to carry out these complex procedures. A new national commissioning goal (CQUIN) to encourage thrombectomy training will also help and I hope to see many local health systems taking advantage of this.
It is good to see the Long Term Plan recognises how effective thrombectomy can be and the potential cost-savings involved. On average, each patient treated with mechanical thrombectomy saves the NHS nearly £50,000 over just five years.

Ending the ‘postcode lottery’ of stroke care

Standards of stroke care today vary enormously across the country, affecting your ability to survive and recover. It is simply not good enough that 45% of stroke survivors feel abandoned after they leave hospital and are not all able to access the rehabilitation and lifelong support that they need. Last month, another CQUIN was introduced, this time to increase the numbers of stroke survivors accessing vital six-month reviews. These will enable stroke survivors to access more personalised support and help to rebuild their lives after stroke.
Equity of access is key here. As James Green, who has lost three of his family members to stroke and now campaigns with the Stroke Association, explains:
“For me, the overriding priority for the new National Stroke Programme is reducing the postcode lottery of care for those who have had a stroke. We must have a level field for everyone no matter where you live or your wealth.”

Priorities for the future

NHS England’s goals for stroke are rightly ambitious and they will require sustained effort and real leadership to drive through improvement. The next five years should be about translating good intentions into action. Together, we must make sure there are tangible improvements for stroke survivors and their carers. We need to be bold and accept where things are not working and design services so that everybody can access world-class stroke care. Stroke survivors deserve a better deal than they are getting today and I and others will continue to push for stroke to be the priority it needs to be.

Juliet Bouverie
Chief Executive
Stroke Association
Tel: +44 (0)300 3300 740

Strokes made NHS boss Phil campaign for better mental health care

So even the NHS chief doesn't understand that depression is a secondary problem. You get people 100% recovered and the secondary problems will likely not be needed to be solved. YOUR responsibility is to educate him. With absolutely NO PROTOCOLS that lead to 100% recovery this depression and PTSD is quite likely.  Solve the correct problem, not this secondary issue.

23% chance of stroke survivors getting PTSD

Poststroke depression(33% chance)


Strokes made NHS boss Phil campaign for better mental health care

Phil on his first visit home from hospital following his two strokes
Phil on his first visit home from hospital following his two strokes

  • Phil Woodford is calling for more psychological support for stroke survivors, after experiencing for himself the difficulty of getting help following two strokes.

    The 48 year old from Catterall says the strokes over one weekend in 2016 left him with post traumatic stress disorder (PTSD), severe depression and feeling suicidal.

    Back on his bike - Phil learns to cycle again following two strokes and his rehabilitation

    Back on his bike - Phil learns to cycle again following two strokes and his rehabilitation

    But he says he was forced to get his own treatment for his mental health problems.
    Phil is now backing a campaign by the Stroke Association calling for more support to cope with hidden and often overlooked psychological and emotional effects of a stroke.
    He said: “A stroke changes not just the survivor’s life overnight but also their family’s. I had never had bad or negative thoughts before but I started feeling suicidal as I couldn’t see much of a future. I couldn’t cope...I was scared, angry, upset and frightened.”
    Keen cyclist Phil, Associate Director of Corporate Affairs at University Hospital of Morecambe Bay NHS Foundation Trust, is now back at work. He was 45 when illness hit in August 2016 and says that although he has not regained all his physical skills it is the mental challenges which have been the hardest to cope with.
    He praises the NHS for the treatment of his stroke but said “I think psychological support and rehab should start as soon as a stroke is diagnosed, to help stroke survivors overcome the emotional impact of their stroke.
    “I saw my GP and told her about the suicidal thoughts and she referred me for mental health support but it was rejected, and they just said to adjust my anti-depressants.
    “I ended up going private to the Priory in Bury and it has been a lifesaver. I have been treated with talking therapies and I feel more positive about the future.
    Phil said: “For a while, I felt like a failure, but I have got over that now.
    “There is one good thing that has come out of the stroke and that is it has made me realise the important things in life. I spend much more time with my children and am happier.”
    He said the Priory helped him recognise he had aspects of PTSD and severe depression: “When the depression comes I just want to crawl into a ball and be alone.”
    He twice planned suicide but said: “I was able to bring myself round by thinking about the good things in my life, especially my family, my dog and friends.”

    After a week at Royal Preston Hospital, Phil made the decision to be transferred to the Royal Lancaster Infirmary for his rehabilitation and spent three months having intensive physiotherapy. It took about a month for him to get his first movements back. When discharged from hospital he was given a package of care at home as he was then unable to wash or dress himself.
    According to new research by the Stroke Association almost a million people who have survived a stroke have developed at least one mental health problem.
    Its report The Lived Experience of Stroke- Hidden Effects is based on a survey of 11,134 stroke sufferers has just been published.

    Tuesday, June 18, 2019

    Brain Activations During Optokinetic Stimulation in Acute Right-Hemisphere Stroke Patients and Hemispatial Neglect: An fMRI Study

    You'll have to hope your doctor can understand and apply this. I have no clue. 

    Back in August 2014 this one failed so have your doctor do an analysis to see why.

    Randomized controlled trial on hemifield eye patching and optokinetic stimulation in acute spatial neglect August 2014

     The latest here:

    Brain Activations During Optokinetic Stimulation in Acute Right-Hemisphere Stroke Patients and Hemispatial Neglect: An fMRI Study 

    First Published June 12, 2019 Research Article

    Objective. Leftward optokinetic stimulation (OKS) is a promising therapeutic approach for right-hemisphere stroke patients with left hemispatial neglect. We questioned whether the putative neural basis is an activation of frontoparietal brain regions involved in the control of eye movements and spatial attention.  
    Methods. We used functional magnetic resonance imaging to investigate brain activations during OKS in acute right-hemisphere stroke patients (RHS, n = 19) compared with healthy control subjects (HC, n = 9). Based on neuropsychological testing we determined the ipsilesional attention bias in all RHS patients, 11 showed manifest hemispatial neglect.  
    Results. In HC subjects, OKS in either direction led to bilateral activation of the visual cortex (V1-V4), frontal (FEF) and supplementary (SEF) eye fields, intraparietal sulcus (IPS), basal ganglia, and thalamus. RHS patients’ activations were generally reduced compared with HC. Nevertheless, leftward OKS bilaterally activated the visual cortex (V1-V4), FEF, SEF, IPS, and thalamus. The neural response to OKS was negatively correlated with patients’ behavioral impairment: The greater the individual attention bias/neglect the weaker the brain activations.  
    Conclusion. In RHS patients, leftward OKS activates frontoparietal regions (FEF, IPS) that are spared from structural brain damage and functionally involved in both oculomotor control and spatial attention. This may provide a neural basis for the known therapeutic effects of OKS on hemispatial neglect. In acute stroke stages, reduced activation levels correlating with neglect severity indicate functional downregulation of the underlying dorsal attention network. Therefore, chronic RHS patients with less severe neglect after recovery of network disturbances may be more suitable candidates for OKS rehabilitation.

    Article available in:

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    The Earliest Signs of Alzheimer’s Everyone Over 50 Should Know

    The Earliest Signs of Alzheimer’s Everyone Over 50 Should Know
    Alzheimer’s—the most common type of dementia—affects millions of Americans. According to a recent study published in the Alzheimer’s Association’s journal Alzheimer’s and Dementia, as many as 5 million Americans were living with the disease in 2014. Unfortunately, since most Alzheimer’s patients are diagnosed after 60 years old, many of its early signs seem like normal age-related issues at first, according to the Centers for Disease Control and Prevention (CDC). But, if left untreated, the condition’s effects extend well beyond occasionally losing keys or forgetting someone’s name. When it comes to Alzheimer’s, every minute counts—so read on to discover the earliest signs of Alzheimer’s that everyone over 50 should know. And for more ways to stay mentally fit as you age, check out these 20 Surprising Habits That Reduce Your Alzheimer’s Risk.
    1. Forgetting the Names of Friends and Family Members
    2. Becoming Totally Uninterested in Everything
    3. Putting Things in Strange Places
    4. Exhibiting Poor Judgement
    5. Forgetting the Names of Everyday Objects
    6. Needing Constant Memory Aids
    7. Getting Lost in Familiar Places
    8. Becoming Aggressive
    9. Becoming Agitated
    10. Becoming Socially Withdrawn
    11. Not Being Able to Keep Track of and Pay Bills
    12. Misplacing Words While Talking
    13. Experiencing Confusion
    14. Having a Shortened Attention Span
    15. Taking Longer to Complete Basic Tasks
    16.  Becoming Suspicious or Distrustful of Others
    17. Sudden Mood Swings
    18. Not Being Able to Follow Recipes
    19. Forgetting Conversations
    20. Wearing Inappropriate Clothing
    21. Not Being Able to Play Familiar Games
    22. Forgetting You've Already Said Something
    23. Finding It Hard to Make Phone Calls
    24. Engaging in Impulsive Behavior
    25. Becoming Unable to Multitask
    Details at link.

    Your doctor needs a protocol to prevent that descent into dementia. I don't care that it doesn't exist today. Your doctor needs to do their job and either create or find one that is effective. 

    Automated and Quantitative Assessment of Tactile Mislocalization After Stroke

    We don't fucking care about your description of a stroke problem. We want solutions. WHEN THE HELL ARE YOU GOING TO PROVIDE THEM?

    Automated and Quantitative Assessment of Tactile Mislocalization After Stroke

    Mike D. Rinderknecht1*, Julio A. Dueñas1, Jeremia P. Held2,3, Olivier Lambercy1, Fabio M. Conti4, Leopold Zizlsperger2,3, Andreas R. Luft2,3, Marie-Claude Hepp-Reymond5 and Roger Gassert1
    • 1Rehabilitation Engineering Laboratory, Department of Health Sciences and Technology, Institute of Robotics and Intelligent Systems, ETH Zurich, Zurich, Switzerland
    • 2Division of Vascular Neurology and Neurorehabilitation, Department of Neurology, University of Zurich and University Hospital Zurich, Zurich, Switzerland
    • 3Cereneo, Center for Neurology and Rehabilitation, Vitznau, Switzerland
    • 4Clinica Hildebrand Centro di Riabilitazione Brissago, Brissago, Switzerland
    • 5Institute of Neuroinformatics, University of Zurich and ETH Zurich, Zurich, Switzerland
    Topesthesia, the recognition of tactile stimulation location on the skin, can be severely affected by neurological injuries, such as stroke. Despite topesthesia being crucial for manipulating objects and interacting with the environment during activities of daily living, deficits cannot be quantitatively captured with current clinical assessments and are, as a consequence, not well-understood. The present work describes a novel automated assessment tool for tactile mislocalization in neurological patients with somatosensory deficits. We present two cases of ischemic stroke patients, describe their tactile localization deficits with the automated assessment, and compare the results to a standard manual clinical assessment. Using the automated assessment tool, it was possible to identify, locate, precisely quantify, and depict the patients' deficits in topesthesia. In comparison, the clinical assessment was not sensitive enough and some deficits would remain undetected due to ceiling effects. In addition, an MRI structural analysis of the lesion supported the existence of somatosensory deficits. This novel and quantitative assessment may not only help to raise awareness of the implications of deficits in topesthesia, but would also allow monitoring recovery throughout the rehabilitation process, informing treatment design, and objectively evaluating treatment efficacy.

    Region-specific and activity-dependent regulation of SVZ neurogenesis and recovery after stroke

    You can have your doctor analyze these 10 pages and come back to you with stroke rehab protocols. I don't care that this is in mice, waiting for human trials will take place after you are dead.

    Region-specific and activity-dependent regulation of SVZ neurogenesis and recovery after stroke

    Huixuan Lianga, Handi Zhaoa, Amy Gleichmana, Michal Machnickia, Sagar Telanga, Sydney Tanga, Mary Rshtounia,Jack Ruddella, and S. Thomas Carmichaela,1aDepartment of Neurology, David Geffen School of Medicine, University of California, Los Angeles, CA 90095Edited by Anders Björklund, Lund University, Lund, Sweden, and approved May 13, 2019 (received for review July 10, 2018)
     Stroke is the leading cause of adult disability. Neurogenesis after stroke is associated with repair; however, the mechanisms regulating post stroke neurogenesis and its functional effect remain unclear. Here, we investigate multiple mechanistic routes of induced neurogenesis in the poststroke brain, using both a fore-limb overuse manipulation that models a clinical neurorehabilitation paradigm, as well as local manipulation of cellular activity in the periinfarct cortex. Increased activity in the forelimb peri-infarct cortex via either modulation drives increased subventricular zone (SVZ) progenitor proliferation, migration, and neuronal maturation in periinfarct cortex. This effect is sensitive to com-petition from neighboring brain regions. By using orthogonal tract tracing and rabies virus approaches in transgenic SVZ lineage tracing mice, SVZ-derived neurons synaptically integrate into the perinfarct cortex; these effects are enhanced with forelimb over-use. Synaptic transmission from these newborn SVZ-derived neurons is critical for spontaneous recovery after stroke, as tetanus neurotoxin silencing specifically of the SVZ-derived neurons disrupts the formation of these synaptic connections and hinders functional recovery after stroke. SVZ-derived neurogenesis after stroke is activity-dependent, region-specific, and sensitive to modulation, and the synaptic connections formed by these newborn cells are functionally critical for post stroke recovery.

    Blood pressure pill has potential to slow down Alzheimer’s disease

    It is YOUR RESPONSIBILITY to get your doctor and stroke hospital involved with followup research into human subjects on this. Your stroke hospital will do nothing if you don't speak up. Because your stroke hospital has done no followup for decades is the reason nothing is ever solved in stroke.  Does your stroke hospital even know that stroke survivors need this?

    1. A documented 33% dementia chance post-stroke from an Australian study?   May 2012.

    2. Then this study came out and seems to have a range from 17-66%. December 2013.

    3. A 20% chance in this research.   July 2013.

    4. Dementia Risk Doubled in Patients Following Stroke September 2018


    Blood pressure pill has potential to slow down Alzheimer’s disease

    Laura Donnelly
    Research found that those given the pills for six months saw a 20 per cent increase in circulation of blood to the hippocampus - Naeblys 
    A cheap blood pressure pill could slow down Alzheimer's disease by improving flow of blood to parts of the brain linked to memory, research suggests.
    Dutch research found that those given the pills for six months saw a 20 per cent increase in circulation of blood to the hippocampus.
    The drug, called Nilvadipine, is among a class of calcium channel blockers, costing less than 50 pence a day, which are commonly prescribed to reduce the risk of high blood pressure.
    Scientists said the findings suggest that the decrease in blood flow in patients with Alzheimer’s disease could be reversed.
    But they said it was too early to say if this could slow down progression of disease.
    The study by Radboud University Medical Centre in Nijmegen, the Netherlands, involved 44 participants, half of which were given nilvadipine with half given a placebo for six months.
    At the study's start and after six months, researchers measured blood flow to specific regions of the brain using a unique magnetic resonance imaging (MRI) technique.
    Study lead author Professor Jurgen Claassen, of Radboud University Medical Centre in Holland, said: "This high blood pressure treatment holds promise as it doesn't appear to decrease blood flow to the brain, which could cause more harm than benefit.
    "Even though no medical treatment is without risk, getting treatment for high blood pressure could be important to maintain brain health in patients with Alzheimer's disease."
    Researchers said sample sizes were too small and follow-up time too short to reliably study the effects of this cerebral blood flow increase on structural brain measures and cognitive measures.
    A larger study involving more than 500 people with mild to moderate Alzheimer's disease did not show the drug had an impact on the condition. However, those with mild symptoms of disease did have a slower decline in memory.
    The condition affects 850,000 people in the UK, of which around six in ten have Alzheimer's disease.
    Dr Laura Phipps, from Alzheimer’s Research UK, said: “We know high blood pressure is a risk factor for developing dementia but it’s unclear whether blood pressure-lowering drugs could improve memory and thinking in people with Alzheimer’s.
    “There is strong evidence that there are things we can do to keep our brain healthy as we age. This includes keeping our blood pressure and cholesterol in check as well as not smoking, only drinking within the recommended limits, eating a balanced diet, and staying mentally and physically active.”

    Monday, June 17, 2019

    Recovery Post-Stroke: Proportional or Not?

    Stroke survivors care not one whit about predictions, they want results. Like EXACT STROKE REHAB PROTOCOLS that deliver 100% recovery. Not guidelines or using subjective measurement tools like Fugl-Meyer. But then I'm stroke addled and obviously have zero say so in how stroke rehab should be done. 

    Recovery Post-Stroke: Proportional or Not?

    Hawe RL, Scott SH, Dukelow SP. Taking Proportional Out of Stroke Recovery. Stroke. 2019;50:204–211.
    In this entry, I discuss a recent publication by Rachel Hawe and colleagues (1) regarding the potential biases of the mathematical properties of the proportional recovery rule and how this may impact application in the field of stroke recovery. Proportional recovery is the idea that most individuals post-stroke (“fitters” to the rule) will recover 70% of their potential on a given outcome (see paper for rule equation). The authors cite multiple studies that have demonstrated proportional recovery for upper limb motor impairment using a single outcome (Fugl Meyer Upper Limb assessment, out of 66 points), and recent work extending this rule to lower limb, aphasia and hemispatial neglect recovery outcomes.
    The principal mathematical concept discussed as a limitation of the proportional recovery rule is mathematical coupling. This concept refers to when one variable directly or indirectly contains all or a part of another. For example, in the case of proportional recovery of the upper limb post-stroke, the initial score on Fugl Meyer Upper Limb assessment is part of both the independent and dependent variables of the proportional recovery rule.
    To demonstrate the impact of mathematical coupling in the context of the proportional recovery rule, the authors present two datasets. First, using simulations of random recovery data (n=200), Hawe et al demonstrate that over 80% of simulations approximate prior proportional recovery findings in terms of slope and R2 values. Second, using data compiled from six published upper limb proportional recovery papers (n = 373 subjects), the authors demonstrate high variability in upper limb recovery (SD=33.4%) despite an R2 of 0.86. Further, the number of subjects displaying ~70% recovery was near chance levels. They subsequently go on to examine the impact of mathematical coupling using other measures (Purdue Pegboard and Functional Independence Measure), highlighting similar issues.
    Predicting recovery after stroke remains a major challenge for the field. Proportional recovery has been suggested to be a benchmark for testing the effect of future interventions. However, such a proposal requires careful consideration of the mathematical limitations raised in the current paper. A very large dataset with common data elements may advance our understanding of prediction in stroke recovery. But, impacting this goal is the limitation of ceiling and floor effects demonstrated in the current paper, emphasizing the need for greater sensitivity in indexing recovery to inform meaningful predictions at the level of the individual stroke survivor.
    This paper is not the first to challenge the proportional recovery rule from a mathematical perspective. A recent paper by Tom Hope and colleagues (2) also discussed the methodological limitations of the proportional recovery rule. Linked to this paper is a letter to the editor from one of the groups that has investigated the proportional recovery rule (3), with a reply from Hawe and colleagues (4) available.
    1. Hawe RL, Scott SH, Dukelow S. Taking proportional out of stroke recovery. Stroke. 2019;50:204-11.
    2. Hope TMH, K. F, Price CJ, Leff AP, Rotshtein P, Bowman H. Recovery after stroke: not so proportional after all? Brain. 2019;142:15-22.
    3. Byblow W, Stinear C. Letter by Byblow and Stinear Regarding Article “Taking Proportional Out of Stroke Recovery”. Stroke. 2019;50:e125.
    4. Hawe RL, Scott SH, Dukelow SP. Response by Hawe et al to Letter Regarding Article, “Taking Proportional Out of Stroke Recovery”. Stroke. 2019;50:e126.

    Chronic inflammation removes motivation by reducing dopamine in the brain

    Is this one of the reasons survivors lack motivation? I would say no, the motivation lack comes directly from your doctor having NO EXACT PROTOCOLS FOR RECOVERY. If your doctor said do 15 million repetitions of this and you will get this result, you would do 15 million repetitions. I've walked 13,955,868 steps in the last 5 years and still no relief from my ankle, toes and leg spasticity. 

    Chronic inflammation removes motivation by reducing dopamine in the brain

    Why do we feel listless when we are recovering from an illness? The answer is, apparently, that low-grade chronic inflammation interferes with the dopaminergic signaling system in the brain that motivates us to do things.
    This was reported in a new paper published in the journal Trends in Cognitive Sciences.
    The research carried out at Emory University explains the links between the reduced release of dopamine in the brain, the motivation to do things, and the presence of an inflammatory reaction in the body. It also presents the possibility that this is part of the body’s effort to optimize its energy expenditure during such inflammatory episodes, citing evidence gathered during their study.
    The authors also published an experimental framework based on computational tools, devised to test the theory.
    The underlying hypothesis is that the body needs more energy to heal a wound or overcome an infection, for instance, both of which are associated with low-grade inflammation. To ensure that energy is available, the brain uses an adaptive technique to reduce the natural drive to perform other tasks which could potentially drain away the energy needed for healing. This is essentially a recalibration of the specialized reward neurons in the motivation center of the brain, so that ordinary tasks no longer feel like they’re worth doing.
    According to the new study, the mechanism of this recalibration is immune-mediated disruption of the dopamine pathway, reducing dopamine release.
    The computational technique published by the scientists is designed to allow experimental measurements of the extent to which low-grade inflammation affects the amount of energy available, and the decision to do something based on the effort needed. This could allow us to better understand why and how chronic inflammatory states cause a lack of motivation in other disease conditions as well, including schizophrenia and depression.
    Andrew Miller, co-author of the study, says, “If our theory is correct, then it could have a tremendous impact on treating cases of depression and other behavioral disorders that may be driven by inflammation. It would open up opportunities for the development of therapies that target energy utilization by immune cells, which would be something completely new in our field.”
    It is already known that immune cells release cellular signaling molecules called cytokines, which affect the functioning of the dopamine-releasing neurons in the area of the brain called the mesolimbic system. This area enhances our willingness to work hard for the sake of a reward.
    Image Copyright: Meletios, Image ID: 71648629 via
    Recently, it was discovered that immune cells also enjoy a unique capability to shift between various metabolic states, unlike other cells. This could affect cytokine release patterns in such a way as to signal the brain to conserve available energy for the use of the immune system.
    These facts were the foundation of the new hypothesis, which explains it in terms of evolutionary adaptation. In the hypothetical early environment, the immune system, faced with abundant microbial and predatory challenges, needed tremendous amounts of energy. It therefore had its own mechanism to signal other body systems, via the mesolimbic dopamine system, to control the use of energy resources during periods when the organism was undergoing severe or sudden stress.
    Modern life is relatively soft and less challenging. With less physical activity, low-grade inflammation is chiefly due to factors such as obesity, chronic stress, metabolic syndrome, aging and other lifestyle illnesses. This could mistakenly cause the mesolimbic dopamine neurons to produce less dopamine. Lower dopamine levels in turn decrease the motivation for work, by reducing the perception of reward while increasing the perception of effort involved. This ultimately conserves energy for use by the immune system.
    Previous studies by Miller as well as other scientists have shown that a high level of immune functioning in association with low levels of dopamine and reduced motivation characterizes some cases of schizophrenia, depression and certain other mental health conditions.
    The scientists do not think these disorders are caused by the low-grade inflammation, but that some people who have these illnesses are hypersensitive to immune cytokines. This could in turn cause them to lose motivation for daily living.
    The scientists are currently performing a clinical trial on people with depression, to test the theory using the computational framework.
    Treadway M. T. et al., (2019). Can’t or Won’t? Immunometabolic Constraints on Dopaminergic Drive. Trends in Cognitive Sciences.

    Sunday, June 16, 2019

    Marijuana Chokes Alzheimer's-Related Brain Regions

    I wouldn't trust anything here. Due to the use of SPECT scans by Dr. Amen they have a  reputation as only being used to deceive. Do you really think neuropsychiatric patients would have normal brains? The selection of patients for this research shows its bias from the start.

    My 13 reasons for marijuana use post-stroke.  

    Don't follow me, I'm not medically trained and I don't have a Dr. in front of my name.


    Marijuana Chokes Alzheimer's-Related Brain Regions

    In a big study of 26,000 people, the hippocampus "choked" on marijuana. (The hippocampus is the brain's memory and learning center.) Marijuana lowered blood flow to levels unseen in any other group. Find out why this strongly suggests higher vulnerability to Alzheimer’s.

    As the U.S. races to legalize marijuana for medicinal and recreational use, a large scale brain imaging study gives reason for caution. Published in the Journal of Alzheimer’s Disease, researchers using single photon emission computed tomography (SPECT), a sophisticated imaging study that evaluates blood flow and activity patterns, demonstrated abnormally low blood flow in virtually every area of the brain, in nearly 1,000 marijuana users compared to healthy controls.

    Marijuana, Alzheimer's & the Hippocampus

    The marijuana users' low blood flow patterns included areas known to be affected by Alzheimer’s pathology such as the hippocampus.

    Continued below image...

    IMAGE LEGEND: Example of a volume rendered brain SPECT image (top down view) of a healthy control compared to an 18-year old daily user of marijuana. While the control subject has symmetric activity, the marijuana user shows overall decreased perfusion.

    All data were obtained for analysis from a large multi-site database, involving 26,268 patients who came for evaluation of complex, treatment resistant issues to one of nine outpatient neuropsychiatric clinics across the United States (Newport Beach, Costa Mesa, Fairfield, and Brisbane, CA, Tacoma and Bellevue, WA, Reston, VA, Atlanta, GA and New York, NY) between 1995-2015. Of these, 982 current or former marijuana users had brain SPECT at rest and during a mental concentration task compared to almost 100 healthy controls. Predictive analytics with discriminant analysis was done to determine if brain SPECT regions can distinguish marijuana user brains from controls brain.

    Low Blood Flow

    Low blood flow in the hippocampus in marijuana users reliably distinguished marijuana users from controls. The right hippocampus during a concentration task was the single most predictive region in distinguishing marijuana users from their normal counterparts. Marijuana use is thought to interfere with memory formation by inhibiting activity in this part of the brain.

    According to one of the co-authors on the study Elisabeth Jorandby, M.D., “As a physician who routinely sees marijuana users, what struck me was not only the global reduction in blood flow in the marijuana users brains, but that the hippocampus was the most affected region due to its role in memory and Alzheimer’s disease."

    May Be Harbingers of Brain Damage

    She continued, "Our research has proven that marijuana users have lower cerebral blood flow than non-users. Second, the most predictive region separating these two groups is low blood flow in the hippocampus on concentration brain SPECT imaging. This work suggests that marijuana use has damaging influences in the brain – particularly regions important in memory and learning and known to be affected by Alzheimer’s.”

    Dr. George Perry, Editor in Chief of the Journal of Alzheimer’s Disease said, “Open use of marijuana, through legalization, will reveal the wide range of marijuana’s benefits and threats to human health. This study indicates troubling effects on the hippocampus that may be the harbingers of brain damage.”


    Felodipine, FDA-Approved for Blood Pressure, Shows Promise in Dementia

    It is YOUR RESPONSIBILITY to get your doctor and stroke hospital involved with initiating research into human subjects on this. Your stroke hospital will do nothing if you don't speak up. Because your stroke hospital has done no followup for decades is the reason nothing is ever solved in stroke.  Does your stroke hospital even know that stroke survivors need this?

    1. A documented 33% dementia chance post-stroke from an Australian study?   May 2012.

    2. Then this study came out and seems to have a range from 17-66%. December 2013.

    3. A 20% chance in this research.   July 2013.

    4. Dementia Risk Doubled in Patients Following Stroke September 2018


    Felodipine, FDA-Approved for Blood Pressure, Shows Promise in Dementia

    At the University of Cambridge, a prescribed drug to treat high blood pressure has shown promise against conditions such as Parkinson's, Huntington's and forms of dementia in studies carried out in mice and zebrafish.

    A common feature of these diseases -- collectively known as neurodegenerative diseases -- is the build-up of misfolded proteins. These proteins, such as huntingtin in Huntington's disease and tau in some dementias, form 'aggregates' that can cause irreversible damage to nerve cells in the brain.

    Autophagy Protects Brain Cells

    In healthy individuals, the body uses a mechanism to prevent the build-up of such toxic materials. This mechanism is known as autophagy, or 'self-eating', and involves 'Pac-Man'-like cells eating and breaking down the materials. However, in neurodegenerative diseases this mechanism is impaired and unable to clear the proteins building up in the brain.

    As the global population ages, an increasing number of people are being diagnosed with neurodegenerative diseases, making the search for effective drugs ever more urgent. However, there are currently no drugs that can induce autophagy effectively in patients.

    Re-purpose Existing Drugs

    In addition to searching for new drugs, scientists often look to re-purpose existing drugs. These have the advantage that they have already been shown to be safe for use in humans. If they can be shown to be effective against the target diseases, then the journey to clinical use is much faster.

    In a study published today in the journal Nature Communications, scientists at the UK Dementia Research Institute and the Cambridge Institute for Medical Research at the University of Cambridge have shown in mice that felodipine, a hypertension drug, may be a candidate for re-purposing.

    Felodipine Seems to Induce Autophagy

    Epidemiological studies have already hinted at a possible link between the drug and reduced risk of Parkinson's disease, but now the researchers have shown that it may be able to induce autophagy in several neurodegenerative conditions.

    A team led by Professor David Rubinsztein used mice that had been genetically modified to express mutations that cause Huntington's disease or a form of Parkinson's disease, and zebrafish that model a form of dementia.

    Mice are a useful model for studying human disease as their short life span and fast reproductive rate make it possible to investigate biological processes in many areas. Their biology and physiology have a number of important characteristics in common with those of humans, including similar nervous systems.

    Felodipine Reduces Sign of Dementia

    Felodipine was effective at reducing the build-up of aggregates in the mice with the Huntington's and Parkinson's disease mutations and in the zebrafish dementia model. The treated animals also showed fewer signs of the diseases.

    Studies in mice often use doses that are much higher than those known to be safe to use in humans. Professor Rubinsztein and colleagues showed in the Parkinson's mice that it is possible to show beneficial effects even at concentrations similar to those tolerated by humans. They did so by controlling the concentrations using a small pump under the mouse's skin.

    First Time Approved Drug Slows Buildup

    "This is the first time that we're aware of that a study has shown that an approved drug can slow the build-up of harmful proteins in the brains of mice using doses aiming to mimic the concentrations of the drug seen in humans," says Professor Rubinsztein. "As a result, the drug was able to slow down progression of these potentially devastating conditions and so we believe it should be trialed in patients."

    "This is only the first stage, though. The drug will need to be tested in patients to see if it has the same effects in humans as it does in mice. We need to be cautious, but I would like to say we can be cautiously optimistic."

    • The study was funded by Wellcome, the Medical Research Council, Alzheimer’s Research UK, the Alzheimer’s Society, Rosetrees Trust, The Tau Consortium, an anonymous donation to the Cambridge Centre for Parkinson-Plus, Open Targets, the Guangdong Province Science and Technology Program, with additional support from the National Institute for Health Research Cambridge Biomedical Research Centre.

    An anti-fatigue drug has had transformative lifestyle benefits for stroke survivors in a clinical trial conducted by HMRI's Dr Andrew Bivard.

    An anti-fatigue drug(modafinal) has had transformative lifestyle benefits for stroke survivors in a clinical trial conducted by HMRI's Dr Andrew Bivard.

    Nothing here suggests that this was written up as a protocol and distributed to all the worlds' stroke hospitals.  I bet your stroke hospital will do nothing with this information, they will wait for SOMEONE ELSE TO SOLVE THE PROBLEM?

    Your hospital takes no responsibility for finding and implementing research that will help survivors. Ask that if you don't believe me. I bet they don't have a staff person monitoring stroke research. 

    I had massive fatigue immediately post stroke and continuing for years. My doctor stupidly said I needed to get more cardiovascularly fit. He never tested my cardio fitness. Three years after my stroke I had a physical where my resting heart rate was 54 at the age of 53. That means my cardiovascular fitness was that of an athlete, even after doing nothing on it for 3 years. Yet I was still completely fatigued everyday.  

    Statistics on stroke fatigue:

    At least half of all stroke survivors experience fatigue Or is it 70%?

    Or is it 40%?


    Video here: On modafinal

    Saturday, June 15, 2019

    Aging in Older Mice Delayed by Giving Enzyme From Younger Mice

    So now you don't have to guess how young your grandchildren have to be to get their blood. You'll just have to wait decades for followup since there is NO LEADERSHIP anywhere in stroke.  Nothing will occur in time to help you. 

    Young Blood Revitalizes the Aging Brain June 2014


    Aging in Older Mice Delayed by Giving Enzyme From Younger Mice

    New research has identified a novel approach to staving off the detrimental effects of aging, according to a study from Washington University School of Medicine in St. Louis.

    Scientists are seeking new ways to extend healthy life spans, and a new study in mice suggests a novel strategy. Researchers at Washington University School of Medicine in St. Louis have shown that supplementing older mice with an enzyme called eNAMPT from younger mice extends life spans in the older mice. The active mouse in the video was given the enzyme; the less active mouse was given saline. The mice are the same age.

    The study suggests that a protein that is abundant in the blood of young mice plays a vital role in keeping mice healthy. With age, levels of this protein decline in mice and people, while health problems such as insulin resistance, weight gain, cognitive decline and vision loss increase. Supplementing older mice with the protein obtained from younger mice appears to slow this decline in health and extend the life spans of older mice by about 16 percent.

    The study is published June 13 in the journal Cell Metabolism.

    The circulating protein is an enzyme called eNAMPT, which is known to orchestrate a key step in the process cells use to make energy. With age, the body's cells become less and less efficient at producing this fuel -- called NAD -- which is required to keep the body healthy. Washington University researchers have shown that supplementing eNAMPT in older mice with that of younger mice appears to be one route to boosting NAD fuel production and keeping aging at bay.

    "We have found a totally new pathway toward healthy aging," said senior author Shin-ichiro Imai, MD, PhD, a professor of developmental biology. "That we can take eNAMPT from the blood of young mice and give it to older mice and see that the older mice show marked improvements in health -- including increased physical activity and better sleep -- is remarkable."

    Imai has long studied aging, using mice as stand-ins for people. Unlike other studies focused on transfusing whole blood from young mice to old mice, Imai's group increased levels of a single blood component, eNAMPT, and showed its far-reaching effects, including improved insulin production, sleep quality, function of photoreceptors in the eye, and cognitive function in performance on memory tests, as well as increased running on a wheel. Imai's group also has shown other ways to boost NAD levels in tissues throughout the body. Most notably, the researchers have studied the effects of giving oral doses of a molecule called NMN, the chemical eNAMPT produces. NMN is being tested in human clinical trials.

    "We think the body has so many redundant systems to maintain proper NAD levels because it is so important," Imai said. "Our work and others' suggest it governs how long we live and how healthy we remain as we age. Since we know that NAD inevitably declines with age, whether in worms, fruit flies, mice or people, many researchers are interested in finding anti-aging interventions that might maintain NAD levels as we get older."

    Imai's research has shown that the hypothalamus is a major control center for aging throughout the body, and it is directed in large part by eNAMPT, which is released into the blood from fat tissue. The hypothalamus governs vital processes such as body temperature, thirst, sleep, circadian rhythms and hormone levels. The researchers have shown that the hypothalamus manufactures NAD using eNAMPT that makes its way to the brain through the bloodstream after being released from fat tissue. They also showed that this eNAMPT is carried in small particles called extracellular vesicles. As levels of eNAMPT in the blood decline, the hypothalamus loses its ability to function properly, decreasing life span.

    In an intriguing finding, Imai and first author Mitsukuni Yoshida, a doctoral student in Imai's lab, showed that levels of eNAMPT in the blood were highly correlated with the number of days the mice lived. More eNAMPT meant a longer life span, and less meant a shorter one.

    The researchers also showed increased life span with delivering eNAMPT to normal old mice. All mice that received saline solution as a control had died before day 881, about 2.4 years. Of the mice that received eNAMPT, one is still alive as of this writing, surpassing 1,029 days, or about 2.8 years.

    "We could predict, with surprising accuracy, how long mice would live based on their levels of circulating eNAMPT," Imai said. "We don't know yet if this association is present in people, but it does suggest that eNAMPT levels should be studied further to see if it could be used as a potential biomarker of aging."

    The study also found sex differences in levels of eNAMPT, with female mice consistently showing higher levels of the enzyme.

    "We were surprised by the dramatic differences between the old mice that received the eNAMPT of young mice and old mice that received saline as a control," Imai said. "These are old mice with no special genetic modifications, and when supplemented with eNAMPT, their wheel-running behaviors, sleep patterns and physical appearance -- thicker, shinier fur, for example -- resemble that of young mice."

    Imai and his colleagues, including co-author Rajendra Apte, MD, PhD, the Paul A. Cibis Distinguished Professor of Ophthalmology and Visual Sciences, noted that eNAMPT also is carried in extracellular vesicles in humans. As such, future studies should be done to investigate whether low levels are associated with disease in aging people and whether supplementing eNAMPT in extracellular vesicles could serve as an anti-aging intervention in older people, they said.

    Reference: Yoshida et al. 2019. Extracellular Vesicle-Contained eNAMPT Delays Aging and Extends Lifespan in Mice. Cell Metabolism. DOI:

    This article has been republished from the following materials. Note: material may have been edited for length and content. For further information, please contact the cited source.

    An open-label randomized pragmatic non-inferiority pilot trial comparing the effectiveness of Curare 30cH against individualized homeopathic medicines in post-stroke hemiparesis

    My God, what stupidity. Homeopathy has exactly no scientific evidence to back it up.  Comparing one useless homeopathic product to another is complete nonsense. And doing it during spontaneous recovery, in my opinion would be considered akin to fraud. Your choice on what to believe. 

    An open-label randomized pragmatic non-inferiority pilot trial comparing the effectiveness of Curare 30cH against individualized homeopathic medicines in post-stroke hemiparesis

    UshaUchatb1AbhijitChattopadhyayc2Anaitulah AhmadMird3MunmunKoleye4SubhranilSahaf5



    Post-stroke hemiparesis is the most common complication following stroke. Due to unsatisfactory results from conventional treatment, alternative treatments including homeopathy are increasingly becoming popular. Curare is the one of the recommended homeopathic medicine prescribed on ‘common symptoms’ of motor paralysis, but has not been researched systematically. We hypothesized that Curare 30cH would be non-inferior to individualized homeopathy (IH) in treatment of post-stroke hemiparesis in the context of standard physiotherapy.


    An open, randomized (1:1), exploratory, two parallel arms, pragmatic, non-inferiority, pilot trial was conducted at the Homoeopathic Materia Medica out-patient departments of National Institute of Homoeopathy (NIH), India on 50 patients comparing the effectiveness of Curare 30CH against IH. Comparative analysis was carried out on the primary outcome to detect non-inferiority by one-tailed t test at alpha = 5% with a prefixed margin (Δ) of 1.0 based on assumption. Oxford muscle strength grading scale and stroke impact scale (SIS) questionnaires were the primary and secondary outcomes respectively; assessed at baseline, after 3 and 6 months of treatment.


    Five subjects dropped out (Curare: 3, IH: 2). Groups were comparable at baseline (all P > 0.01). In both groups, both the outcomes improved significantly after 3 and 6 months. Non-inferiority was demonstrated by Curare 30cH against IH, both over 3 months (mean difference = 0.04, lower 95% confidence limit -0.195, t = 7.429, P < 0.001) and 6 months (mean difference = -0.2, lower 95% confidence limit -0.474, t = 4.899, P < 0.001). No adverse events were reported from either group.


    Both therapies seemed to produce comparable effects, and appeared as safe, still, being a pilot trial, no definite conclusion could be drawn. Further exploration of both efficacy and effectiveness of either of the therapies is necessary by adequately powered trials and independent replications.
    Trial registration: CTRI/2017/05/008532; UTN: U1111-1196-3761.


    Post-stroke hemiparesis
    Non-inferiority trial
    Reader, Dept. of Homoeopathic Materia Medica, National Institute of Homoeopathy, Block GE, Sector III, Salt Lake, Kolkata 700106, West Bengal, India.
    Professor and Head, Dept. of Homoeopathic Materia Medica, National Institute of Homoeopathy, Block GE, Sector III, Salt Lake, Kolkata 700106, West Bengal, India.
    Former Postgraduate Trainee, Dept. of Homoeopathic Materia Medica, National Institute of Homoeopathy, Block GE, Sector III, Salt Lake, Kolkata 700106, West Bengal, India.
    Independent Researcher; Champsara, Baidyabati, Hooghly 712222, West Bengal, India.
    Independent Researcher; 93/2/1, Shibpur Road, Shibpur, Howrah 711102, West Bengal, India.