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 438 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:

Wednesday, October 22, 2014

Unbroken: A chronic fatigue patient’s long road to recovery

Whom is going to take on this challenge and see if the fatigue experienced by stroke patients might have the same basis? crickets?

Scientists say National Alzheimer’s Plan research milestones must be strengthened

We don't even have a National Stroke Plan because our stroke associations are falling down on the job.

Alzheimer's disease will strike 1 out of 6 older women, study says

Compare that to;

The WHO says women have a 1 in 5 chance of getting a stroke 

Everything in stroke is totally f*cked up, we don't have any strategy or plan on how to tackle all the problems. If we did we could at least comment on it and point out deficiencies.

With no plan no one has to take responsibility, damnable chickenshits.

The Alzheimers stuff here:

2014 Report on the Milestones for the US National Plan to Address Alzheimer's Disease

Concentrate! How to tame a wandering mind

If we are going to recover under the current lack of stroke rehab protocols we are going to have to be completely focused on all the work it is going to take to recover. This should be a mandatory prescription from your doctor until they actually come up with useful rehab protocols. Test yourself at bottom.
Procrastinate often? Caroline Williams does, so decided to find out if brain training could tackle her wandering mind. What she discovered could help everyone.
I am about to be zapped in the head with an electromagnet, once a second, for eight minutes. I fidget, trying to get comfortable in a huge black chair with jointed metal arms that stand between me and the door. I feel faintly ridiculous wearing a tight headband with what looks like a coat hook on the top. “All you need to do is relax,” says Mike Esterman, the researcher about to zap me. That’s easy for him to say – he’s holding the magnet.
"Willpower is like a muscle. I'm a big believer in that." — Tim Pychyl, psychologist
I’ve come to the Boston Attention and Learning Lab in the US to try and train my brain to focus better. Esterman and fellow cognitive neuroscientist Joe DeGutis have spent nearly seven years working on a training programme to help wandering minds stay “in the zone”.

Find out your ‘continuous concentration’ score at I got 53, which is below average. How well do you focus?

more at link.

Vessel occlusion, penumbra, and reperfusion – translating theory to practice

Read it and weep, for our doctors still have no idea what is going on with stroke or how to treat it.
Bruce C. V. Campbell1,2*, imageGeoffrey A. Donnan2 and imageStephen M. Davis1
  • 1Department of Medicine, Royal Melbourne Hospital, University of Melbourne, Parkville, VIC, Australia
  • 2Florey Institute of Neuroscience and Mental Health, University of Melbourne, Parkville, VIC, Australia
The management of ischemic stroke is at a critical juncture. Administration of intravenous tPA is currently restricted to within 4.5 h from stroke onset with several trials in longer time windows proving neutral (1, 2). Revascularization success with tPA in major vessel occlusion is widely recognized as suboptimal (3). Alternative thrombolytic agents with theoretical efficacy advantages such as tenecteplase and desmoteplase are yet to show benefit in phase 3 trials. The promise of endovascular therapy has also yet to translate into positive randomized trials (46), although a new generation of devices is currently being studied. While it is possible that these therapeutic approaches are simply ineffective, the heterogeneity of stroke pathophysiology is likely to be contributing to the neutral results we often observe.
Imaging selection has been proposed as a means of reducing heterogeneity by identifying patients with the potential to benefit from revascularization and therefore enhancing the probability of success in trials of new therapies. However, whether it is sufficient to demonstrate an occluded artery as the target or to also require evidence of salvageable downstream tissue has been debated. The recent announcement of neutral results in DIAS 3 (7), a trial that compared desmoteplase versus placebo 3–9 h after stroke onset in patients with vessel occlusion, without reference to downstream tissue status other than what was visible on non-contrast CT, will no doubt further stimulate this discussion. It is, therefore, salient to consider the current methods to identify salvageable ischemic penumbra and the potential value of commonly used surrogates for clinical outcome, chiefly reperfusion, recanalization, and infarct growth.

Management of fatigue in persons with multiple sclerosis

At least they have something. For stroke we have absolutely nothing. ASA, NSA, WSO are you going to step up to the plate and do the required research to solve the fatigue issue after stroke?

Regional white matter damage predicts speech fluency in chronic post-stroke aphasia

I really don't give a shit about predictions, I want to know what the solution is to fix the aphasia problem. It's really quite simple, solve the damned stroke problems, don't just describe them.
Alexandra Basilakos1*, imagePaul T. Fillmore1, imageChris Rorden2, imageDazhou Guo1, imageLeonardo Bonilha3 and imageJulius Fridriksson1
  • 1The Aphasia Lab, Department of Communication Sciences and Disorders, University of South Carolina, Columbia, SC, USA
  • 2Department of Psychology, University of South Carolina, Columbia, SC, USA
  • 3Department of Neurosciences, Medical University of South Carolina, Charleston, SC, USA
Recently, two different white matter regions that support speech fluency have been identified: the aslant tract and the anterior segment of the arcuate fasciculus (ASAF). The role of the ASAF was demonstrated in patients with post-stroke aphasia, while the role of the aslant tract shown in primary progressive aphasia. Regional white matter integrity appears to be crucial for speech production; however, the degree that each region exerts an independent influence on speech fluency is unclear. Furthermore, it is not yet defined if damage to both white matter regions influences speech in the context of the same neural mechanism (stroke-induced aphasia). This study assessed the relationship between speech fluency and quantitative integrity of the aslant region and the ASAF. It also explored the relationship between speech fluency and other white matter regions underlying classic cortical language areas such as the uncinate fasciculus and the inferior longitudinal fasciculus (ILF). Damage to these regions, except the ILF, was associated with speech fluency, suggesting synergistic association of these regions with speech fluency in post-stroke aphasia. These observations support the theory that speech fluency requires the complex, orchestrated activity between a network of pre-motor, secondary, and tertiary associative cortices, supported in turn by regional white matter integrity.

More at link.

New Research on Walnuts and the Fight Against Alzheimer’s Disease

How long before walnuts are added to your hospital diet? 100 years? What is the downside of doing this right now?
My diet here: I'll have to add walnuts.

What would a post-stroke diet look like? 

Animal study reveals potential brain-health benefits of a walnut-enriched diet
A new animal study published in the Journal of Alzheimer’s Disease indicates that a diet including walnuts may have a beneficial effect in reducing the risk, delaying the onset, slowing the progression of, or preventing Alzheimer’s disease.
Research led by Abha Chauhan, PhD, head of the Developmental Neuroscience Laboratory at the New York State Institute for Basic Research in Developmental Disabilities (IBR), found significant improvement in learning skills, memory, reducing anxiety, and motor development in mice fed a walnut-enriched diet.
The researchers suggest that the high antioxidant content of walnuts (3.7 mmol/ounce)1 may have been a contributing factor in protecting the mouse brain from the degeneration typically seen in Alzheimer’s disease. Oxidative stress and inflammation are prominent features in this disease, which affects more than five million Americans2.
“These findings are very promising and help lay the groundwork for future human studies on walnuts and Alzheimer’s disease – a disease for which there is no known cure,” said lead researcher Dr. Abha Chauhan, PhD. “Our study adds to the growing body of research that demonstrates the protective effects of walnuts on cognitive functioning.”
The research group examined the effects of dietary supplementation on mice with 6 percent or 9 percent walnuts, which are equivalent to 1 ounce and 1.5 ounces per day, respectively, of walnuts in humans. This research stemmed from a previous cell culture study3 led by Dr. Chauhan that highlighted the protective effects of walnut extract against the oxidative damage caused by amyloid beta protein. This protein is the major component of amyloid plaques that form in the brains of those with Alzheimer’s disease.
Someone in the United States develops Alzheimer’s disease every 67 seconds, and the number of Americans with Alzheimer's disease and other dementias are expected to rapidly escalate in coming years as the baby boom generation ages. By 2050, the number of people age 65 and older with Alzheimer's disease may nearly triple, from five million to as many as 16 million, emphasizing the importance of determining ways to prevent, slow or stop the disease. Estimated total payments in 2014 for all individuals with Alzheimer’s disease and other dementias are $214 billion2.
Walnuts have other nutritional benefits as they contain numerous vitamins and minerals and are the only nut that contains a significant source of alpha-linolenic acid (ALA) (2.5 grams per ounce), an omega-3 fatty acid with heart and brain-health benefits4,5. The researchers also suggest that ALA may have played a role in improving the behavioral symptoms seen in the study.

A rich vocabulary can protect against cognitive impairment

So is your doctor prescribing vocabulary work?

Some people suffer incipient dementia as they get older. To make up for this loss, the brain's cognitive reserve is put to the test. Researchers from the University of Santiago de Compostela have studied what factors can help to improve this ability and they conclude that having a higher level of vocabulary is one such factor.

'Cognitive reserve' is the name given to the brain's capacity to compensate for the loss of its functions. This reserve cannot be measured directly; rather, it is calculated through indicators believed to increase this capacity.

A research project at the University of Santiago de Compostela (USC) has studied how having a wide vocabulary influences cognitive reserve in the elderly.

As Cristina Lojo Seoane, from the USC, co-author of the study published in the journal 'Anales de Psicología' (Annals of Psychology), explains to SINC: "We focused on level of vocabulary as it is considered an indicator of crystallised intelligence (the use of previously acquired intellectual skills). We aimed to deepen our understanding of its relation to cognitive reserve."

The research team chose a sample of 326 subjects over the age of 50 - 222 healthy individuals and 104 with mild cognitive impairment. They then measured their levels of vocabulary, along with other measures such as their years of schooling, the complexity of their jobs and their reading habits.

They also analysed the scores they obtained in various tests, such as the vocabulary subtest of the 'Wechsler Adult Intelligence Scale' (WAIS) and the Peabody Picture Vocabulary Test.

"With a regression analysis we calculated the probability of impairment to the vocabulary levels of the participants," Lojo Seoane continues.
The results revealed a greater prevalence of mild cognitive impairment in participants who achieved a lower vocabulary level score.
"This led us to the conclusion that a higher level of vocabulary, as a measure of cognitive reserve, can protect against cognitive impairment," the researcher concludes.

Flu Vaccine May Hold Key to Preventing Heart Disease

And may be helpful for stroke also.

Seasonal flu vaccine may cut stroke risk

 Flu Vaccine May Hold Key to Preventing Heart Disease

 A new study in Vaccine explains how flu vaccines prevent heart attacks

Flu vaccines are known to have a protective effect against heart disease, reducing the risk of a heart attack. For the first time, this research, published in Vaccine, reveals the molecular mechanism that underpins this phenomenon. The scientists behind the study say it could be harnessed to prevent heart disease directly.

Heart disease is the leading cause of death worldwide. People can reduce their risk of heart disease by eating healthily, exercising and stopping smoking. However, to date there is no vaccine against heart disease.

Previous clinical findings show that people that receive the seasonal flu vaccine also benefit from its protective effect against heart disease; the risk of having a heart attack in the year following vaccination is 50% lower than people who did not receive the vaccination. The exact mechanism underlying this protective effect remained unknown.

This new study for the first time reveals this mechanism, showing that the flu vaccine stimulates the immune system to produce antibodies that switch on certain processes in cells. These processes lead to the production of molecules that protect the heart. The researchers say that based on the results it may be possible to develop a new vaccine against heart disease.

"Even though the protective effect of the flu vaccine against heart disease has been known for some time, there is very little research out there looking at what causes it. Our proposed mechanism could potentially be harnessed in a vaccine against heart disease, and we plan to investigate this further," said Dr. Veljkovic, Institute Vinca, Belgrade, the lead author of the new study.

The researchers identified a protein called the bradykinin 2 receptor (BKB2R), which is involved in cellular processes that protect the heart. Some of the antibodies the body produces after flu vaccination switch this protein on, therefore protecting against heart disease. The researchers analysed 14 flu viruses used in vaccines, and identified four that could be investigated for use in potential heart disease vaccines.

"The rate of administering flu vaccinations is disappointingly low, even in developed countries," added Dr. Veljkovic "We hope that our results will encourage more people to get vaccinated before the flu season starts."


Clinical trial could change standard treatment for stroke

Whom is going to consolidate all this and create a damned f*cking stroke protocol?
 You are going to have to remember all this and immediately post-stroke question your doctors to see if they know what they are doing. You better hope you are not unconscious.

Someday our medical teams will figure out exactly what should be done for blood pressure lowering post-stroke. Maybe create a f*cking protocol and publish it for the world to see. Other research here:

1. Detrimental effect of blood pressure reduction in the first 24 hours of acute stroke onset
2. Early Intensive Blood-Pressure Lowering Improves Recovery in Patients With Acute Intracerebral Haemorrhage
 3.  Systolic Blood Pressure During Acute Stroke Is Associated With Functional Status and Long-term Mortality in the Elderly
 4. External Counterpulsation Augments Blood Pressure and Cerebral Flow Velocities in Ischemic Stroke Patients With Cerebral Intracranial Large Artery Occlusive Disease
5.  The One Benefit Of High Blood Pressure? It May Prevent Dementia
6.  Stopping Pre-Stroke Antihypertensive Medication Advised During Acute Stroke 
7.  Mild induced hypertension improves blood flow and oxygen metabolism in transient focal cerebral ischemia
8.  Low Diastolic Pressure Linked to Brain Atrophy 
9.  New Treatment for Stroke Set to Increase Chances of Recovery - haemorrhage blood pressure lowering
The latest here: 
A large international clinical trial has shed new light on the effectiveness of current hospital protocols for managing blood pressure in stroke patients.
The two-part ENOS trial (Efficacy of Nitric Oxide in Stroke,) was carried out at The University of Nottingham in collaboration with 23 countries to try to solve two major conundrums faced by doctors when treating people who have suffered a stroke — should blood pressure be lowered using medicated skin patches, and should existing blood pressure medication be stopped or continued after a stroke?
The results of the trial, carried out by the University’s Stroke Trial Unit in the Division of Clinical Neurosciences, are being published in The Lancet.
The trial was funded by the Medical Research Council, Efficacy and Mechanism Evaluation (EME) Programme, and BUPA Foundation.
The trial involved 4,011 patients with acute stroke, both ischaemic (blood clot) and haemorrhagic (bleeding). Patients were randomly assigned to receive a glyceryl trinitrate 5mg skin patch (often used in angina patients) or no patch for 7 days. Patients who were already on medication for high blood pressure before their stroke were also randomly assigned to either continue or stop this for 7 days after the stroke.
Leading the trial, Stroke Association Professor of Stroke Medicine Philip Bath, said:  “We found that in patients with acute stroke and high blood pressure, treatment with glyceryl trinitrate patches had acceptable safety but did not improve functional outcome. But there seemed to be benefit in patients who were treated very early, within 6 hours of the onset of symptoms. We aim to carry out a further, larger trial testing very early treatment with the skin patch.
“Our results also show that there is no evidence to support the policy of continuing pre-stroke blood pressure-lowering medication in the acute phase of stroke. An adverse effect in the group continuing medication was pneumonia in patients who had difficulty swallowing, perhaps due to inhalation of the medication into the lungs. Furthermore, discharge home, disability and cognition were all less favourable in those who were allocated to continue BP treatment immediately.”
Professor Bath added: “Our results suggest that antihypertensive treatment should be continued once a patient who has suffered a stroke is stable and is able to swallow medications safely. But there appears to be no urgency to restart treatment in the first week.
“Some doctors in the emergency department seem to feel obliged to get a stroke patient back on their blood pressure medication as soon as possible, but our trial implies they should not rush it.”
The ENOS trial results were initially presented by Professor Bath at the European Stroke Association annual conference in May 2014.

Mindfulness and you

Just in case you want to try this. I am 100% certain you won't hear about this from your doctor. But don't do this dangerous meditation without your doctors ok.

Mindfulness-Based Cognitive Therapy

Mindfulness-Based Stress Reduction

7 Myths About Mindfulness

Mindfulness exercises

Quotes About Mindfulness

20 Awesome Quotes about Mindful Living

Mindfulness-Based Cognitive Therapy for Depression






Effects of tea intake on blood pressure: a meta-analysis of 21 randomized controlled trials

In case you want to know what your tea habit does for you.
Other benefits of tea here;

Black Tea Linked with Reduced Risk of Heart Attack, Stroke and Tooth Decay

Interactions of black tea polyphenols with human gut microbiota: implications for gut and cardiovascular health

Polyphenols from green tea prevent antineuritogenic action of Nogo-A via 67-kDa laminin receptor and hydrogen peroxide

Green Tea Boosts Your Brain

Green Tea Or Coffee May Reduce Stroke Risk

Green Tea Boosts Memory 




Liu Gang; Huang Xiaohong
J Am Coll Cardiol. 2014;64(16_S):. doi:10.1016/j.jacc.2014.06.519
text A A A
To read this abstract, download the PDF from the toolbox at the top right.
The effect of tea intake on blood pressure (BP) is controversial. We undertook a meta-analysis of randomized controlled trials to determine changes in systolic and diastolic BP due to the intake black and green tea.
MEDLINE, EMBASE, and the Cochrane Controlled Trials Register were searched from 1966 until January 2014 for studies in parallel group or crossover design in which BP was assessed before and after receiving black or green tea for at least 1 week. The weighted mean difference was calculated for net changes in BP by using fixed-effects or random-effects models. Previously defined subgroup analyses were performed to explore the influence of study characteristics.
21 eligible randomized controlled trials with 1323 subjects were enrolled. After the tea intake, the pooled mean systolic and diastolic BP were −1.8 mmHg (95% confidence interval [CI], −2.4- −1.1 mmHg) and −1.4mmHg (95% CI, −2.2- −0.6 mm Hg) lower, respectively, compared with the tea-free controls. Subgroup analyses showed that the BP-lowering effect was apparent in the subjects who consumed a tea over a median of 12 weeks (systolic/diastolic BP, -2.6/-2.1 mmHg, both P <0.001). Stratified by type of tea, green tea significantly reduced systolic and diastolic BP of -2.1 (95% CI, −2.9- −1.2) and -1.7 (95% CI, −2.9- −0.5) mm Hg, and black tea significantly reduced systolic and diastolic BP of -1.4 (95% CI, −2.4- −0.4) and -1.1 (95% CI, -1.9- −0.2) mm Hg, respectively. The benefits of tea intake were not influenced by ethnicity, treatment dose of tea catechins, individual health status, or caffeine intake.
The meta-analysis showed that long-term (≥12 weeks) ingestion of a tea (green and black tea) resulted in a significant reduction in systolic and diastolic BP.


Stress May Be Harder On Women’s Hearts Than Men’s

So is your doctor treating your chance of  PTSD following stroke of 23%. more agressively? What is your doctor doing to relieve the stress of having no stroke protocols to get back to 100% recovery? Or the worry about your 33% dementia chance post-stroke from an Australian study?
Researchers have known for decades that stress contributes to heart disease. But a new analysis by researchers at Duke Medicine shows mental stress may tax women’s hearts more than men’s. 
The research appears online Oct. 13, 2014, in the Journal of the American College of Cardiology.
“Normally when under stress, we fight back or run away. In order to do that, we need to pump more blood to the body,” said Wei Jiang, M.D., the study’s senior author and professor of medicine, psychiatry and behavioral sciences at the Duke University School of Medicine. “According to the data, women were not reacting that way as well as men were.”
In their analysis, Duke researchers reviewed data on 254 men and 56 women who had a history of ischemic heart disease or decreased blood flow to the heart. The group was part of a Duke study published in 2012 called REMIT, which evaluated the impact of an anti-depressant medicine to reduce stress-induced heart trouble.
Participants performed stressful tasks, such as describing an event that made them angry, while researchers monitored their heart function and other vital signs.
During times of stress, 57 percent of female participants experienced reduced blood flow to the heart, or ischemia, as compared to 41 percent of men. Ischemia is a prevalent component of cardiovascular disease and often the factor that leads to death.
Differences between the sexes could provide clues on how to tailor heart disease education, prevention and treatment for women and men. Heart disease kills about 600,000 people each year and remains the leading cause of death in the U.S. for both men and women, according to the Centers for Disease Control. 
But studies have shown disparities in the outcomes of ischemic heart disease, with women faring worse than men. CDC surveys have found disparities in women’s awareness of heart disease risks, and how quickly women seek treatment for their symptoms.
In the Duke study, women under mental stress expressed a greater increase in negative emotions and a greater decrease in positive feelings. By contrast, men had greater rise in blood pressure in response to mental stress, the data showed.
“Men may have been expressing less changes in emotions, but they had an obvious negative physiologic response to stress,” said Zainab Samad, M.D., M.H.S., the study’s lead author and assistant professor of medicine at Duke.
The data also found sex distinctions in blood platelet behavior. The aggregation of platelets can lead to a blockage that could cause a heart attack. Despite the use of medications designed to keep blood platelets from clustering together, the platelets of female participants under mental stress were still clumping to a greater extent than those of male participants. 
Samad said that with further research, this detail could help tailor blood-thinning medications for more effective use in women.
“The impact of negative physiologic responses to mental stress needs to be recognized in cardiovascular risk assessment in both sexes," Samad said. "These differences may be potential reasons for differences in outcomes, and may also serve as avenues for further research. This could be a signal that we have been looking for to treat heart disease better, especially in women.”
In addition to Jiang and Samad, study authors included Stephen Boyle; Mads Ersboll; Amit N. Vora; Ye Zhang; Richard C. Becker; Redford Williams; Cynthia Kuhn; Thomas L. Ortel; Joseph G. Rogers; Christopher O’Connor; and Eric J. Velazquez.
The National Heart, Lung, and Blood Institute provided grant support (RO1HL085704).

Regulatory T Cells in Central Nervous System Injury: A Double-Edged Sword

I don't understand, but what is your doctor doing with this information?


Previous research investigating the roles of T effector (Teff) and T regulatory (Treg) cells after injury to the CNS has yielded contradictory conclusions, with both protective and destructive functions being ascribed to each of these T cell subpopulations. In this work, we study this dichotomy by examining how regulation of the immune system affects the response to CNS trauma. We show that, in response to CNS injury, Teff and Treg subsets in the CNS-draining deep cervical lymph nodes are activated, and surgical resection of these lymph nodes results in impaired neuronal survival. Depletion of Treg, not surprisingly, induces a robust Teff response in the draining lymph nodes and is associated with impaired neuronal survival. Interestingly, however, injection of exogenous Treg cells, which limits the spontaneous beneficial immune response after CNS injury, also impairs neuronal survival. We found that no Treg accumulate at the site of CNS injury, and that changes in Treg numbers do not alter the amount of infiltration by other immune cells into the site of injury. The phenotype of macrophages at the site, however, is affected: both addition and removal of Treg negatively impact the numbers of macrophages with alternatively activated (tissue-building) phenotype. Our data demonstrate that neuronal survival after CNS injury is impaired when Treg cells are either removed or added. With this exacerbation of neurodegeneration seen with both addition and depletion of Treg, we recommend exercising extreme caution when considering the therapeutic targeting of Treg cells after CNS injury, and possibly in chronic neurodegenerative conditions.

Feasibility study of the effects of art as a creative engagement intervention during stroke rehabilitation on improvement of psychosocial outcomes: study protocol for a single blind randomized controlled trial: the ACES study

But is this better than music and music training? Intelligent stroke patients want to know.
Dammit, create some f*cking stroke protocols so they can be evaluated as to what works and doesn't work. Quit relying on the shitworthy statement, 'All strokes are different, all stroke recoveries are different'.



Benefits of art participation after stroke are becoming increasingly recognized. Qualitative studies suggest that participation in visual arts creative engagement interventions (CEIs) during rehabilitation after stroke may improve mood, self-esteem, hope and some aspects of physical recovery. This study examines the feasibility of undertaking a randomized controlled trial of a CEI delivered by artists within in-patient stroke rehabilitation to test effectiveness.


This trial is a two arm, single-blind, randomized controlled feasibility trial within in-patient stroke rehabilitation. We will recruit 80 patients receiving stroke rehabilitation in two stroke units in a health board area of Scotland (40 patients in each arm). Intervention arm participants will receive a visual-arts based CEI facilitated by experienced artists. Artists will follow an intervention protocol with specific components that enable participants to set, achieve and review artistic goals. Participants will receive up to eight intervention sessions, four within a group and four one-to-one with the artist. Control group participants will receive usual care only.Data collection will occur at baseline, post-intervention and three-month follow-up. Stroke-related health status is the primary outcome; mood, self-esteem, self-efficacy, perceived recovery control and hope are secondary outcomes. Semi-structured interviews will be conducted with purposively selected patients, artists and healthcare staff to elicit views and experiences of the intervention and feasibility and acceptability of trial processes. Recruitment rates, retention rates and patient preference for art participation will also be collected. Data will indicate, with confidence intervals, the proportion of patients choosing or refusing participation in the CEI and will allow calculation of recruitment rates for a future definitive trial. Summary data will indicate potential variability, magnitude and direction of difference between groups. Findings will inform sample size calculations for a definitive trial. Thematic analysis of qualitative data will be managed using the Framework Approach. Framework is an analytical approach for qualitative data, commonly used in policy and medical research.


If shown to demonstrate effects, this intervention has the potential to address aspects of stroke recovery previously. Not routinely addressed in rehabilitation.


Registered with Clinical Trials.Gov: NCT02085226 on 6th March 2014.

Starting Primary Prevention Earlier With Statins

You can check out the atherosclerotic cardiovascular disease (ASCVD) calculator here:
ASCVD Risk Estimator
My 10 year risk is 4.7%, lifetime is 46%.
According to this I should not need to be on statins, but then I discontinued them on my own 4 years ago. Never follow anything I do, I'm stroke-addled.

Starting Primary Prevention Earlier With Statins


The 2013 American College of Cardiology/American Heart Association Guideline on the Treatment of Blood Cholesterol to Reduce Atherosclerotic Cardiovascular Risk in Adults was based on a systematic review of randomized trials with atherosclerotic cardiovascular disease (ASCVD) outcomes and meta-analyses of these trials published through 2011. With evidence of an ASCVD risk reduction benefit greatly outweighing the potential for adverse effects, the guideline recommends statin therapy for primary prevention in those with ≥7.5% 10-year ASCVD risk and consideration of statin therapy in those with 5% to <7.5% 10-year ASCVD risk. Subsequent meta-analyses of the statin trials support these recommendations and have additionally found a reduction in total mortality in lower-risk subjects. Additional evidence from imaging trials and epidemiologic studies suggests that initiation of statin therapy earlier in the course of ASCVD could have the potential to more effectively prevent age-related progression of atherosclerosis. Given the high levels of suboptimal risk factors in adults and the safety and availability of low-cost generic statins, a consideration of all the available evidence strongly supports earlier intervention for the primary prevention of ASCVD. In conclusion, earlier initiation of statin therapy has the potential to have a large long-term impact on the heavy burden of cardiovascular disease in the aging populations.

Hollywood Treatment for the Rehabilitation of Facial Palsy and Stroke Patients

Maybe something for your doctor to consider.

Britain's largest conference bringing together experts from the reconstructive, cosmetic and non-surgical worlds witnessed this weekend the unveiling of new technology to help treat facial paralysis; developed by a plastic surgeon and the animation teams that worked on blockbusters such as Harry Potter, The Mummy, bestselling video game Grand Theft Auto and the L'Oréal 'Makeup Genius' app.
Revolutionary new iPad software to aid the rehabilitation of patients with facial palsy conditions including those stemming from strokes was introduced to an audience of more than 3,000 surgeons, doctors and nurses at the Clinical Cosmetic and Reconstructive Expo in London Olympia, 10-11 October, 2014.
The project, which is part-funded by the Wellcome Trust is a collaboration between researchers at the Queen Victoria Hospital in East Grinstead, Brighton-based technology company Sense Innovation, and Image Metrics, a leading film computer graphics company in Manchester. Past facial animation credits of Image Metrics include Harry Potter, The Mummy, and The Curious Tale of Benjamin Button, starring a reversely-ageing Brad Pitt.
Facial palsy is a debilitating condition in which the muscles in the face are weakened, causing a variety of symptoms ranging from numbness to total paralysis of the features. Facial palsy can be caused by a variety of factors, including infections such as Bell's palsy or Lyme Disease, neurological conditions, strokes and developmental syndromes.

More at link.

Tuesday, October 21, 2014

Long Considered a Threat, Viagra May Help Treat Heart Disease

And why not use it for stroke?
This made it sound helpful, even though it was just in rats and during the first week:

Viagra and stroke rehab
Does your doctor know anything at all about your stroke rehab in the first week?

Science Shows How Piano Players' Brains Are Actually Different From Everybody Elses'

And if we had anything approaching a great stroke association we would be researching pianists that had a stroke and see how well they recover. But NO, we have crap for stroke associations.

Design of micro and nanoparticles to improve treatments for Alzheimer's and Parkinson's

If this is possible for other diseases we should have some stroke researchers smart enough to use this in treating stroke deficits. What is your doctor doing about this?

Cold sores increases the risk of dementia

And is your doctor addressing this along with your 33% dementia chance post-stroke from an Australian study?  I remember having cold sores as a kid.
Infection with herpes simplex virus increases the risk of Alzheimer's disease. Researchers at Umeå University, Sweden, claim this in two studies in the journal Alzheimer’s & Dementia.
"Our results clearly show that there is a link between infections of herpes simplex virus and the risk of developing Alzheimer's disease. This also means that we have new opportunities to develop treatment forms to stop the disease," says Hugo Lövheim, associate professor at the Department of Community Medicine and Rehabilitation, Geriatric Medicine, Umeå University, who is one of the researchers behind the study. 
Alzheimer's disease is the most common among the dementia diseases. In recent years research has increasingly indicated that there is a possible connection between infection with a common herpes virus, herpes simplex virus type 1, and Alzheimer's disease.  A majority of the population carries this virus.  After the first infection the body carries the virus throughout your lifetime, and it can reactivate now and then and cause typical mouth ulcer. The hypothesis which links the herpes virus and Alzheimer's disease is based on that a weakened immune system among the elderly creates opportunities for the virus to spread further to the brain.  There this can in turn start the process which results in Alzheimer's disease.
Hugo Lövheim and Fredrik Elgh, professor at the Department of Virology, have now confirmed this link in two large epidemiological studies.  In one study, which is based on the Betula project, a study on ageing, memory and dementia, the researchers show that a reactivated herpes infection doubled the risk of developing Alzheimer's disease. This study had 3,432 participants who were followed for 11.3 years on average.  In another study, samples donated to the Medical Biobank at Umeå University from 360 people with Alzheimer's disease were examined and as many matched people who had not developed dementia.  The samples were taken on average 9.6 years before diagnosis.  This study showed an approximately doubled risk of developing Alzheimer's disease if the person was a carrier of the herpes virus.
"Something which makes this hypothesis very interesting is that now herpes infection can in principle be treated with antiviral agents. Therefore within a few years we hope to be able to start studies in which we will also try treating patients to prevent the development of Alzheimer's disease," says Hugo Lövheim.

Local Muscle Injection of Botulinum Toxin Type A Synergistically Improves the Beneficial Effects of Repetitive Transcranial Magnetic Stimulation and Intensive Occupational Therapy in Post-Stroke Patients with Spastic Upper Limb Hemiparesis

Have your doctor read this. I'm getting tired of pouring the same types of information into my brain.
Are they even considering that spasticity occurs in about 30% of patients?
Yamada N. · Kakuda W. · Kondo T. · Mitani S. · Shimizu M. · Abo M.

aDepartment of Rehabilitation Medicine, Jikei University School of Medicine, Minato-Ku, Tokyo and bShimizu Hospital, Kurayoshi, Tottori, Japan


Background: The purpose of this study was to determine whether local injection of botulinum toxin type A (BoNT-A) into the spastic muscles has any added benefits to repetitive transcranial magnetic stimulation (RTMS)/occupational therapy (OT) in patients with spastic upper limb hemiparesis. Methods: The study subjects of 80 post-stroke patients with spastic upper limb hemiparesis (age: 60.2 ± 13.0 years, time after stroke: 55.3 ± 43.0 months), were divided into the BoNT-A plus RTMS/OT group and RTMS/OT group. BoNT-A was injected into the spastic muscles (total dose: 240 units) before RTMS/OT. The latter included 12 sessions of 40 min RTMS over the non-lesional hemisphere and 240-min intensive OT daily over 15 days. Spasticity was evaluated by the modified Ashworth scale (MAS) and the motor function of the affected upper limb was evaluated serially with Fugl-Meyer Assessment and Wolf Motor Function Tests. Results: Both groups showed significant improvements in spasticity and motor function. The addition of BoNT-A resulted in better improvement in FMA score and MAS of finger flexor muscles (p < 0.05). Conclusions: The triple-element protocol of local injection of BoNT-A into spastic finger muscles, RTMS and intensive OT, is a promising therapeutic program for post-stroke spastic upper limb hemiparesis, although its significance should be confirmed in randomized, placebo-controlled trials

New test to help brain injury victims recover

Will this be enough for your doctor to create stroke protocols to address your cognitive problems post-stroke?
  • New SPANS assessment can help patients suffering from traumatic brain injury, aneurism, dementia, stroke and more between ages 18-74
  • Test suitable for measuring concentration, memory retention, motor performance, language skills and spatial awareness in patients
A dynamic new assessment for helping victims of trauma to the brain, including those suffering from progressive conditions such as dementia, has been developed by a clinical neuropsychologist at the University of Leicester.
The Short Parallel Assessments of Neuropsychological Status (SPANS) is the brainchild of Dr Gerald Burgess from the University of Leicester’s School of Psychology and has been designed to engage with patients suffering from a variety of brain injuries in order to aid in their recovery.
SPANS is unique in that it measures the cognitive skills of individuals with acquired brain injury and progressive neurological conditions in a user-friendly and concise way, taking patients an estimated 35 minutes to complete.
The assessment is capable of measuring seven key cognitive skills: orientation, attention and concentration, language, memory and learning, visuo-motor performance, efficiency and conceptual flexibility.
An alternate version is available, SPANS B, which complements SPANS A for reliable retesting of patients.
Both versions were developed based upon real neurological syndromes, such as aphasia, and common referral questions informed by Dr Burgess’s experience as a clinical psychologist in brain injury wards.
Dr Burgess said: “With SPANS clinicians now have a broader and more reliable assessment that is even more useful than most tests for tracking changes in cognitive skills over time. Patients are now more thoroughly assessed by a test that is less taxing on them than some other tests, so that their difficulties may be better understood.”
The test is suitable to be administered by a range of healthcare professionals, including clinical or research psychologists, occupational therapists, speech and language therapists, psychiatrists and neurologists.
During the development of SPANS Dr Burgess worked with Hogrefe, the publisher, who helped in collecting data and developing SPANS to a professional standard through production and marketing efforts.
Mr Roley Davis, Sales & Marketing Manager at Hogrefe said: “We are proud to have worked with Dr Burgess to bring this innovative new assessment to the market.  SPANS is a comprehensive and flexible test that will address the various needs of clinicians and researchers alike.  Hogrefe’s mission is to develop robust, valid and reliable assessments that address market need, and the SPANS is an excellent addition to our clinical portfolio. We look forward to hearing from people interested to know more about the assessment.”
For more information about SPANS visit Hogrefe’s website here:
A paper about the development and use of SPANS is available here:

Want To Train Your Brain To Feel More Compassion? Here’s How

You might want the social workers at the hospital to train your relatives and friends in compassion towards you rather than judging you for not being who you used to be.

World Stroke Day - Only a Few Days Away!

An email from the National Stroke Association where they don't even acknowledge that everything in stroke is totally f*cked up.  If you don't even know you have a problem there is no way you can ever fix it.

Mr. Matt Lopez as Next CEO,  you have your work cut out for you. Lots to fix in your organization if you are to fulfill your mission statement.

Stroke Advocacy Network - Take Action

Dear dean,
Send an email to your representativesThe national and international effects of stroke are clear. In the United States, 795,000 people will experience a stroke every year. Globally, stroke will claim six million lives annually. World Stroke Day is right around the corner and we are still pushing members of Congress support the U.S. and global stroke community, but we need your help.
Congress has the ability to better the lives of stroke survivors and their loved ones, but some members of Congress are unaware of stroke’s prevalence. Please contact your legislators today and ask them to submit a statement to the record recognizing World Stroke Day. By promoting this international stroke awareness day, your legislators will learn more about the impact that stroke has on the lives of those in the stroke community.
Advocates from all over the nation are already reaching out to their members of Congress. Join your fellow advocates and contact your legislators today.
Contact your representatives in Congress with pre-written messages (which you can personalize). Help us help the entire stroke community—it only takes a minute to make a big difference!
Signature of Angie Baker
Angie Baker
Manager, Policy Advocacy 

 0. There is no fast, easy and objective way to diagnose a stroke.
1. tPA may save your life but only has a 12% efficacy for full recovery.
2. Your neurologist doesn't have any concrete stroke protocols to save all the neurons that are dying in the first week.
3. Your neurologist or physiatrist doesn't have any clue about how to get you to full recovery. (Ask them exactly how to do it), you'll get excuses.
4. Only 10% get to full recovery.
5. No protocols to prevent your 33% chance of getting dementia post-stroke.
6. Nothing to alleviate your fatigue.
7. Nothing that will cure your spasticity.
8. Nothing on cognitive training unless you find this yourself.
9. No published stroke protocols.
10. No way to compare your stroke hospital results vs. other stroke hospitals.
Everything in stroke is a complete failure. 

Personality Traits Predict the Onset of Disease

I'm sure your doctor is following this news and up-to-date on research. That would then entail telling you you need to change your personality to reduce your risk of disease.
Abstract here;
More readable article here;
The Best Personality Trait For Your Health

asthma drug, Xolair - Omalizumab May Elevate Risk of Cardiovascular, Cerebrovascular Adverse Events

Be careful out there.
A review of safety studies by the US Food and Drug Administration (FDA) suggests a slightly increased risk of cardiovascular and cerebrovascular adverse events among patients being treated with the asthma drug omalizumab (Xolair) than in those who were not treated with the drugs.
As a result, the FDA has added information about these potential risks to the drug label.
The review found no difference in the rates of cancer between those patients being treated with omalizumab and those who were not being treated with omalizumab. However, due to limitations in the 5-year study, the FDA cannot rule out a potential risk of cancer with omalizumab, so this information was added to the Warnings and Precautions section of the drug label.
Information for healthcare professionals:
• The FDA has added information about the findings of a slightly elevated risk of cardiovascular and cerebrovascular serious adverse events in omalizumab -treated patients to the Adverse Reactions section of the omalizumab label. The FDA has also added information about uncertain findings regarding a potential risk of cancer to the Warnings and Precautions section of the drug label.
• Periodically reassess the need for continued therapy with omalizumab based on the patient’s disease severity and level of asthma control.
• The appropriate duration of therapy for chronic idiopathic urticaria has not been evaluated. Periodically reassess the need for continued omalizumab therapy.
• Instruct patients receiving omalizumab not to decrease the dose or stop taking the drug or any other asthma medicines unless you instruct them to do otherwise.
• Provide and instruct patients to read the omalizumab patient Medication Guide before starting treatment and before starting each new prescription.
• Report adverse events involving omalizumab to the FDA MedWatch program.
Healthcare professionals and patients are encouraged to report adverse events or side effects related to the use of these products to the FDA's MedWatch Safety Information and Adverse Event Reporting Program:

Monday, October 20, 2014

How the Brain Rewires After Stroke - UCLA 2006

It is only 8 years old from UCLA. How is your doctor using this knowledge and updated protocols to help you recover? Has your doctor understood this at all?
Recent advances have provided vital clues that shed light on how the brain repairs and rewires itself, facilitating recovery from stroke. "We're beginning to understand exactly how the brain repairs itself after stroke," says S. Thomas Carmichael, M.D., UCLA neurologist. "We are identifying time windows in which certain repair processes are active.
Dr. Carmichael and researchers in his lab are studying the molecular and cellular mechanisms of axonal sprouting and stem cell responses to brain injury, and how these two processes of neuronal regeneration lead to repair of damaged brain circuits.
Using imaging techniques, researchers have determined that most of the recovery after stroke occurs in the tissues that border the nerve cells that die due to lack of blood supply and oxygen. In addition, researchers discovered which gene systems mediate the axonal sprouting. These findings offer two important clues about the biology of stroke recovery.
The brain operates as a set of circuits that control movement, thinking, emotion and behavior. A stroke interrupts or kills off certain circuits, causing debilitating paralysis as well as speech and cognitive problems and behavioral and emotional changes. Some spontaneous recovery does occur, however. For example, a patient may be unable to move his or her left side at all immediately following a stroke. Over time, usually about six months, some function returns. The circuits nearest the area damaged by the stroke naturally form new connections, routing around the damage and resulting in this recovery. "What is happening is the brain is remapping and reorganizing itself, and that is where recovery is occurring," Dr. Carmichael explains. "What we're trying to determine is if we can improve and enhance that recovery."
His research team found that nervous system injury induces expression of both growth-promoting and growth-inhibitory genes that together determine the location and degree of axonal sprouting. In the past, the extent of a patient's recovery depended upon the severity of the stroke. But new therapeutics may be able to boost the axonal sprouting process, allowing for the formation of more connections.
The brain could reroute its processes around the dead cells to restore more function. Children who suffer from stroke recover fully because their brains are still developing and are in a more plastic state, better able to make the circuit connections needed for repair. As humans grow and develop into adults, their brains solidify and lose that ability.
For years, researchers debated whether the adult brain could remap itself the way younger brains do. After researchers proved this did happen in adults, the second critical step was to find out how. As it turns out, the gene expression associated with axonal sprouting in the adult brain after stroke is unique, not like the axonal sprouting found in the peripheral or developing nervous systems. "This may give us clues as to why the adult brain is not as successful at rewiring itself as the peripheral and developing nervous system is," Dr. Carmichael says. "Obviously, most adult stroke patients don't recover well enough after stroke to resume normal function, yet children do. The fact that there is a unique growth program in the adult brain suggests that there may be unique targets at which we can aim new therapeutics."
Dr. Carmichael and his researchers are working to identify molecular targets to promote a neuronal growth program and induce increased axonal sprouting after stroke. Patients are taken through therapies that force them to walk more, use their arms more, or challenge their language function more completely. However, there are no drugs now that can be used to induce improved recovery after stroke.
"There needs to be a combination approach," Dr. Carmichael says. "If we were to develop a drug that enhanced sprouting, we could use that drug in combination with physical therapies that are the traditional mainstay of stroke rehabilitation."
The long-term goal is to move neurological rehabilitation closer to the acute stroke and marry the treatment of recovery to the treatment of the stroke itself.
"Epidemiological evidence has shown that most motor and sensory recovery is finished by the six-month mark," Dr. Carmichael says. "The goal of the molecular studies in stroke rehabilitation is to move the start of neural repair closer to the acute stroke itself, and to extend this limited time window for recovery well beyond six months."
Recommended Reading
Carmichael ST (2006) Cellular and molecular mechanisms of neural repair after stroke: making waves. Annal Neurol. 59:725-742.

Scientific Evidence Does Not Support 'Brain Game' Claims

Well shit. What are we supposed to do for our cognitive training to reduce our chances of getting dementia? What does your doctor suggest?
Ask for something specific. Not this crap statement, 'All strokes are different, all stroke recoveries are different'.
The Stanford Center for Longevity joined today with the Max Planck Institute for Human Development in issuing a statement skeptical about the effectiveness of so-called "brain game" products. Signing the document were 69 scholars, including six from Stanford and cognitive psychologists and neuroscientists from around the world.
Laura Carstensen, a Stanford psychology professor and the director of the Center for Longevity, said as baby boomers enter their golden years, commercial companies are all too often promising quick fixes for cognition problems through products that are unlikely to produce broad improvements in everyday functioning.
More at link.

Sunday, October 19, 2014

How to Feel Happy Just By Walking Differently

Is your doctor going to recommend this instead of treating your depression?

What good is it to do research and make new discoveries when no one pays any attention to the findings?

A quote from Musings of a Dinosaur
This is so true of stroke research. I don't know how many thousands of times I've pointed to research that looks like it might be useful to stroke patients and I bet not a single one of them has been implemented in any stroke doctors practice. We may as well go back to blood letting as a stroke prescription as discussed in the 1843 book, 'An Essay On The Nature and Treatment of Apoplexy'.
Ask your doctor why they haven't gone back to blood letting since they really haven't followed any later research?

Exploring a Neuroplasticity Model of Music Therapy

Don't just explore it, come up with a stroke protocol.
  1. Elizabeth L. Stegemöller, PhD, MT-BC
+ Author Affiliations
  1. Iowa State University
  1. Address correspondence concerning this article to Elizabeth L. Stegemöller, 240 Forker, Department of Kinesiology, Iowa State University, Ames IA, 50011.


Background: Given that music therapists work across a wide range of disabilities, it is important that therapists have at least a fundamental understanding of the neurophysiology associated with the client/patient populations that they serve. Yet, there is a large gap of evidence regarding the neurophysiological changes associated with applying music as therapy.

Objective: The purpose of this article is to provide music therapists with a general background in neuroplasticity principles that can be applied to the use of music therapy with multiple populations.

Methods: This article will review literature on neuroplasticity and literature supporting the specific attributes of music therapy that apply to neuroplasticity. Finally, examples of how to use neuroplasticity principles to explain and support clinical music therapy will be provided.

Results: Using the material presented in this review, music therapists will be equipped with information to effectively communicate why music therapy works using three neuroplasticity principles; increase in dopamine, neural synchrony, and a clear signal.

Conclusion: Music therapy is a powerful tool to enhance neuroplasticity in the brain.