Deans' stroke musings

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

What this blog is for:

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

Sunday, April 23, 2017

4 foot wide sidewalks are not wide enough

Saw the MET opera Eugene Onegin today. Afterwards went to a friends house where three of us consumed 3 bottles of wine. Got home about 10:30, still needed 3300 steps yet to complete my totals for the week. I kinda swayed and took over the complete 4 foot width of the sidewalk to get those steps in.   Finally grabbed my walking stick and completed the trails in the dark in the woods nearby. I'm obsessed with completing 70,000 steps per week. So far 25 weeks in a row. It has allowed me to lose 10 pounds and keep my wine and social engagements up. 

Saturday, April 22, 2017

Microvascular endothelial dysfunction can predict dementia

Is this one of the tests your doctor is doing so that the dementia prevention protocol can be implemented in full force?

(HealthDay)—Markers of microvascular endothelial dysfunction can predict dementia, according to a study published online April 13 in the Journal of Internal Medicine.
Hilma Holm, from Lund University in Malmö, Sweden, and colleagues examined the longitudinal association of midregional pro-atrial natriuretic peptide (MR-proANP), C-terminal endothelin-1 (CT-proET-1), and midregional pro-adrenomedullin (MR-proADM) with in a population-based cohort of 5,347 individuals without prevalent dementia (age, 69 ± 6 years).
Over a period of 4.6 ± 1.3 years, 373 patients were diagnosed with dementia. The researchers found that there were significant associations for higher levels of MR-proANP with increased risk of all-cause and (hazard ratio per one standard deviation, 1.2 and 1.52, respectively). Across quartiles of MR-proANP, there was an increase in the risk of all-cause dementia (hazard ratio, 1.83 for quartile 4 versus 1), which was most pronounced for vascular type (hazard ratio, 2.71). Vascular dementia was predicted by the two highest quartiles of CT-proET-1, with a cut-off value at 68 pmol/L (hazard ratio, 1.94 for quartiles 3 to 4 versus 1 to 2). After adjustment for traditional risk factors, elevated levels of MR-proADM indicated no increased risk of developing dementia.
"Elevated plasma concentration of MR-proANP is an independent predictor of all-cause and vascular dementia," the authors write. "Pronounced increase in CT-proET-1 indicates higher risk of vascular dementia."
More information: Abstract
Full Text (subscription or payment may be required)

Journal reference: Journal of Internal Medicine search and more info website

Post-stroke epilepsy

Only out since 2001. Has your doctor done one goddamn thing about this problem since then? Only 27 references to back this up, has your doctor read even one of them?
  • Tom Skyhøj Olsen
  • Tom Skyhøj Olsen
    • 1
  1. 1.Department of NeurologyGentofte University HospitalHellerupDenmark
DOI: 10.1007/s11883-001-0029-4
Cite this article as:
Olsen, T.S. Curr Atheroscler Rep (2001) 3: 340. doi:10.1007/s11883-001-0029-4


Seizures occur in about 10% of stroke patients. Hence, stroke is the most common cause of seizures and epilepsy in the elderly population. Five percent are early-onset seizures (peak onset within the first day after the stroke) and another 5% are late-onset seizures (peak onset within 6 to 12 months after the stroke). Epilepsy (ie, recurrent seizures) develops in 3% to 4% of the stroke patients (in about one third of the patients with early-onset seizures and about one half of the patients with late-onset seizures). There is a strong positive correlation between stroke severity and the risk of post-stroke seizures; the risk is very low in mild strokes. Seizures are more common in hemorrhagic stroke and in stroke with cortical involvement. Whether this is due to the hemorrhagic component or the cortical involvement per se, or a reflection of more severe strokes among patients with hemorrhagic strokes and lesions involving cortical structures, is not clear. The influence of seizures on outcome is still a matter of controversy. Although epileptic seizures are considered easy to control, this is not supported by evidence from randomized controlled trials.

Preventing Seizure-Caused Damage to the Brain

You may have to worry about this. Ask your doctor for details.
Seizures occur in about 10% of stroke patients. Hence, stroke is the most common cause of seizures and epilepsy in the elderly population.
You don't need more damage after your stroke, so demand your doctor prevent that damage.  What researchers are your doctors collaborating with to solve this in humans?
Summary: Exosomes isolated from mesenchymal stem cells can limit brain damage caused by status epilepticus, a new study reports.
Source: Texas A&M.
New research from the Texas A&M College of Medicine points to a potential way to protect neurons.
Tiny vesicles isolated from adult mesenchymal stem cells and administered intranasally can limit the damage to the brain of animal models caused by a seizure disorder called status epilepticus, according to research published this week in the Proceedings of the National Academy of Sciences (PNAS).
Status epilepticus is the formal name for a single seizure lasting longer than 30 minutes or a series of seizures in which the person doesn’t regain consciousness in between them. If it is not quickly stopped, even one episode can cause brain damage, loss of cognitive function and memory loss.
“Saving the brain from injury and disease is certainly one of the holy grails of medicine,” said Darwin J. Prockop, MD, PhD, the Stearman Chair in Genomic Medicine, professor at the Texas A&M College of Medicine and co-senior author of the article. “Our paper suggests one way that this might be done, and not by a procedure that requires brain surgery or even injection into a vein: All that would be required is a nasal spray that a patient might receive in a doctor’s office.”
The compound in the nasal spray is anti-inflammatory exosomes, or extracellular vesicles, which Prockop and his team isolated from cultures of mesenchymal stem cells, a type of adult stem cell.
Ashok K. Shetty, PhD, a professor at the Department of Molecular and Cellular Medicine at the Texas A&M College of Medicine, associate director of the Institute for Regenerative Medicine, research career scientist at the Olin E. Teague Veterans Medical Center and co-senior author of the paper, and his team tested the efficiency of these exosomes in a status epilepticus model with damage from a period of acute seizures. “What is remarkable is that the animal models were rescued from long-term effects of the seizure-induced brain injury by a nasal spray of exosomes,” Prockop said. It was able to ease inflammation of the neurons, prevent cognitive and memory dysfunction and stop abnormal neurogenesis in the hippocampus, a vital part of the brain responsible for memory.
“We gave the intranasal vesicle spray twice over 24 hours, the first one at two hours after the onset of a status epilepticus episode, and such treatment was effective at reducing multiple adverse effects on the hippocampus,” said Shetty. “In fact, the vesicles were able to move to the hippocampus in six hours, and their neuroprotection was enough to prevent loss of normal cognitive and memory function as well as abnormal neurogenesis, one of the substrates involved in formation of new memories.”
Drugs like benzodiazepines, which are tranquilizers, and hydantoins, a type of anticonvulsant, are used to stop status epilepticus episodes, but they are often unavailable—especially if the person hadn’t previously been diagnosed with epilepsy, which is the case 75 percent of the time—and they are ineffective perhaps as much as 30 percent of the time. “There really hasn’t been anything noninvasive like this to stop the cascade of inflammation and abnormal neuronal wiring or epileptogenesis that occurs after a status epilepticus event,” Shetty said. “These vesicles do seem able to protect the brain after seizures, stop neuroinflammation and prevent the development of chronic epilepsy that often results without this treatment.”
Image shows neurons.
The compound in the nasal spray is anti-inflammatory exosomes, or extracellular vesicles, which Prockop and his team isolated from cultures of mesenchymal stem cells, a type of adult stem cell. image is credited to Ashok K. Shetty.
Although the findings are promising, the researchers urge caution before jumping to conclusions about a treatment for humans with seizures.
“Before this therapy can safely be tested in patients, we need to do great deal of further work,” said Prockop, who is also the director of the Texas A&M College of Medicine Institute for Regenerative Medicine. “But the inflammation in the brain caused by acute seizures is similar to the inflammation seen in the late stages of other brain diseases, including Alzheimer’s disease, parkinsonism, multiple sclerosis and traumatic injuries,” Shetty added. “Therefore, the promise of this new therapy is enormous.”
About this neuroscience research article
Source: Holly Shive – Texas A&M
Image Source: image is credited to Ashok K. Shetty.
Original Research: Full open access research for “Intranasal MSC-derived A1-exosomes ease inflammation, and prevent abnormal neurogenesis and memory dysfunction after status epilepticus” by Qianfa Long, Dinesh Upadhya, Bharathi Hattiangady, Dong-Ki Kim, Su Yeon An, Bing Shuai, Darwin J. Prockop, and Ashok K. Shetty in Neuron. Published online April 10 2017 doi:10.1073/pnas.1703920114
Cite This Article
Texas A&M “Preventing Seizure-Caused Damage to the Brain.” NeuroscienceNews. NeuroscienceNews, 21 April 2017.

Parkinson's Disease at 200 Two centuries after its discovery, it's still incurable—but research is accelerating, with major help from citizen scientists in the patient community

We have absolutely NOTHING like this in stroke because we have NO STRATEGY AND NO LEADERSHIP. Your children and grandchildren will still be screwed after having a stroke because of the fucking incompetence and failures of our stroke associations.
Call up your billionaire friends, stroke is solvable, I can get it done.
5 million people living with Parkinsons. 10 million survivors a year for stroke and since only 10% almost fully recover we have 9 million persons a year living with stroke.  And yet we have blithering idiots that say that stroke is currently treatable.

World Stroke Day - Oct. 29 - Failure in full display

Parkinson's Disease at 200

Can Tomatoes Harm Your Digestive System After 50?

I don't have time to listen to this doctor bloviate and with no transcript I won't do it.
I have written  17 posts on tomatoes, mostly positive. Go ask your doctor. Your doctor should know the exact quantity, raw or cooked tomatoes needed per bodyweight and sex to have the proper circulation amount of lycopene in your body for the best benefits. Not knowing that is pure incompetence. Not even collaborating with a researcher on that is even worse incompetence of the stroke department head. The rot may go all the way to the president and the board of directors. So replace them all.

Can Tomatoes Harm Your Digestive System After 50?

Dr. Gundry reveals how tomatoes and other so-called “health foods” may rob you of your energy, ruin your digestive system, and fatten your waistline.

Early glycemic control with metformin cuts CVD events for diabetes patients

You might want to ask your doctor about this.

(HealthDay)—For patients with type 2 diabetes who initiate metformin, early achievement of low hemoglobin A1c (HbA1c) is associated with a reduction in the subsequent risk of cardiovascular events or death, according to a study published online April 12 in Diabetes Care.
Elisabeth Svensson, Ph.D., from Aarhus University Hospital in Denmark, and colleagues conducted a population-based study involving 24,572 metformin initiators with HbA1c tests in Northern Denmark from 2000 to 2012 (median follow-up, 2.6 years). Patients were classified by HbA1c achieved at six months after metformin initiation and by the magnitude of change in HbA1c from the pretreatment base.
The researchers found that, compared with a target HbA1c of <6.5 percent, the risk of a combined outcome event (acute myocardial infarction, stroke, or death) increased gradually with increasing levels of HbA1c achieved (adjusted hazard ratios, 1.18 for 6.5 to 6.99 percent; 1.23 for 7.0 to 7.49 percent; 1.34 for 7.5 to 7.99 percent, and 1.59 for ≥8 percent). Outcome was also predicted by a large absolute HbA1c reduction from baseline (adjusted hazard ratio, 0.80 for Δ = −4, compared with no change [Δ = 0]).
"A large initial HbA1c reduction and achievement of low HbA1c levels within six months after initiation are associated with a lower risk of and death in patients with type 2 diabetes," the authors write.
Several authors disclosed financial ties to Novo Nordisk, which partially funded the study.
More information: Abstract
Full Text

Journal reference: Diabetes Care search and more info website

Subjective perceived impact of Tai Chi training on physical and mental health among community older adults at risk for ischemic stroke: A qualitative study

What useless research. Subjective rather than objectively measuring the health benefits.
Was blood pressure reduced?
How did you measure better mood?
How was energy measured?
This qualitative study intended to assess the perceived benefits of Tai Chi practice among community older population. The researchers indicate that in terms of improved physical health and mental state, regular Tai Chi exercise may have positive benefits among community elderly population, and may be helpful and feasible body–mind exercise to community elderly population for its positive effects and advantages.


  • The researchers conducted this study with participants from a trial examining the effects of a 12-week Tai Chi training on ischemic stroke risk in community older adults (n = 170).
  • Regarding their perceived benefit on physical and mental health and whether Tai Chi exercise was suitable for the elderly, 20 participants were randomly selected from a convenience sample of participants who had completed 12-week Tai Chi training (n = 68) were interviewed.


  • In this study, all participants admitted that Tai Chi training could relax their body and make them comfortable.
  • The greater part of them thought Tai Chi training could promote physical health, including relieving pain, enhancing digestion, strengthening immunity, enhancing energy and improving sleep quality, enhancing their mental and emotional state (e.g. improving mood and reducing anxiety, improving concentration and promoting interpersonal relationship).
  • Also, most of the participants agreed that for community older people, Tai Chi exercise was appropriate.
  • From the content analysis, 3 primary themes emerged: Improving physical health; Enhancing mental and emotional state; Conforming with the request of the elderly.

The effects of object height and visual information on the control of obstacle crossing during locomotion in healthy older adults

Is your physical therapist including this complication in your walking protocols? I had nothing higher than a 2x4, I needed a 18-24 inch high barrier to get over, right now that height and higher I regularly have to do on my walks until I can cut thru the trees


  • In familiar settings, feedforward visual control is similar in young/older adults.
  • Older adults exhibit increased dependence on vision for postural stability.
  • LTC and TTC are correlated when crossing obstacles ≤ 10 cm high regardless of age.


In order to safely avoid obstacles, humans must rely on visual information regarding the position and shape of the object obtained in advance. The present study aimed to reveal the duration of obstacle visibility necessary for appropriate visuomotor control during obstacle avoidance in healthy older adults. Participants included 13 healthy young women (mean age: 21.5 ± 1.4 years) and 15 healthy older women (mean age: 68.5 ± 3.5 years) who were instructed to cross over an obstacle along a pressure-sensitive pathway at a self-selected pace while wearing liquid crystal shutter goggles. Participants were evaluated during three visual occlusion conditions: (i) full visibility, (ii) occlusion at T-1 step (T: time of obstacle crossing), and (iii) occlusion at T-2 steps. Toe clearances of both the lead and trail limb (LTC and TTC) were calculated. LTC in the occlusion at T-2 steps condition was significantly greater than that in other conditions. Furthermore, a significant correlation was observed between LTC and TTC in both groups, regardless of the condition or obstacle height. In the older adult group alone, step width in the occlusion at T-2 steps condition increased relative to that in full visibility conditions. The results of the present study suggest that there is no difference in the characteristics of visuomotor control for appropriate obstacle crossing based on age. However, older adults may exhibit increased dependence on visual information for postural stability; they may also need an increased step width when lacking information regarding their positional relationship to obstacles.

Post-ischemic stroke rehabilitation is associated with a higher risk of fractures in older women: A population-based cohort study

Well shit of course there will be a higher risk. You're teaching them to walk again, That carries a good risk of falling, probably not covered in the release form signed.

  • Huei Kai Huang, 
  • Shu Man Lin, 
  • Clement Shih Hsien Yang, 
  • Chung Chao Liang, 
  • Hung Yu Cheng



Rehabilitation can improve physical activity after stroke. However, patients may be more prone to falls and fractures because of balance and gait deficits. Few reports have studied the relationship between rehabilitation and subsequent fractures after ischemic stroke.


To investigate whether post-stroke rehabilitation affects fracture risk.


We conducted a population-based retrospective cohort study based on the Taiwan National Health Insurance Research Database. Patients with a newly diagnosed ischemic stroke between 2000 and 2012 were included. After propensity score matching, a total of 8,384 patients were enrolled. Half of the patients (4,192) received post-stroke rehabilitation within 1 month; the other half did not receive any post-stroke rehabilitation. Cox proportional hazards regression model was used to calculate hazard ratios (HRs) for fractures among patients with and without rehabilitation within 1 year after ischemic stroke. Patients were further stratified by sex and age (20–64 and ≥65 years).


Patients receiving post-stroke rehabilitation had a higher incidence of fracture (6.2 per 100 person-years) than those who did not (4.1 per 100 person-years) after adjustment for sociodemographic and coexisting medical conditions [HR = 1.53, 95% confidence interval (CI) = 1.25–1.87, p < 0.001]. The analyses performed after stratifying for sex and age showed that only older women undergoing rehabilitation had a significantly higher risk of fracture (HR = 1.62, 95% CI = 1.21–2.17, p = 0.001).


Rehabilitation after ischemic stroke is associated with an increased fracture risk in older women.

Friday, April 21, 2017

J-shaped relationship between habitual coffee consumption and 10-year (2002-2012) cardiovascular disease incidence: The ATTICA study

If I can I drink 4-5 cups of coffee a day. For these other reasons:

Regular coffee drinkers have 'cleaner' arteries March 2015 


Caffeine may counter age-related inflammation


Coffee May Lower Your Risk of Dementia 


Drinking Coffee Can Lower Alzheimer's Risk By 20%, All It Takes Is 3 Cups A Day

J-shaped relationship between habitual coffee consumption and 10-year (2002-2012) cardiovascular disease incidence: The ATTICA study

European Journal of Nutrition
Kouli GM, et al.
The objective of the study portrayed in this paper was to assess the relationship between coffee intake and 10–year cardiovascular disease (CVD) incidence in the ATTICA study, and whether this is modified by the presence or absence of metabolic syndrome (MetS) at baseline. This information supports the protective impact of drinking moderate quantities of coffee (equivalent to approximately 1–2 cups daily) against CVD incidents. This protective impact was only significant for participants without MetS at baseline.


  • A sum of 3042 healthy adults (1514 men and 1528 women) living in the greater area of Athens were voluntarily selected to the ATTICA study amid 2001–2002.
  • In 2011–2012, the 10–year follow–up was performed in 2583 participants (15% of the participants were lost to follow–up).
  • Coffee intake was evaluated by a validated food–frequency questionnaire at baseline (abstention, low, moderate, heavy).
  • Incidence of fatal or non–fatal CVD event was recorded utilizing WHO–ICD–10 criteria and MetS was characterized by the National Cholesterol Education Program Adult Treatment panel III (revised) criteria.


  • Overall, after controlling for potential CVD risk factors, the multivariate examination uncovered a J–shaped relationship between daily coffee drinking and the risk for a first CVD event in a 10–year period.
  • Especially, the odds ratio for low (<150 ml/day), moderate (150–250 ml/day) and heavy coffee intake (>250 ml/day), compared to abstention, were 0.44 (95% CI 0.29–0.68), 0.49 (95% CI 0.27–0.92) and 2.48 (95% CI 1.56–1.93), respectively.
  • This inverse association was also verified among participants without MetS at baseline, but not among participants with the MetS.

Association between active commuting and incident cardiovascular disease, cancer, and mortality: prospective cohort study

I biked to work for 27 years prior to my stroke, 4 miles each way 9 months out of the year.
Still had a stroke, that was not enough to keep my arteries clear. I'm sure that my cardiovascular fitness was what allowed me to survive my stroke.
BMJ 2017; 357 doi: (Published 19 April 2017) Cite this as: BMJ 2017;357:j1456
  1. Carlos A Celis-Morales, research associate1,
  2. Donald M Lyall, research associate2,
  3. Paul Welsh, senior lecturer1,
  4. Jana Anderson, research associate2,
  5. Lewis Steell, postgraduate student1,
  6. Yibing Guo, postgraduate student1,
  7. Reno Maldonado, postgraduate student1,
  8. Daniel F Mackay, reader2,
  9. Jill P Pell, professor2,
  10. Naveed Sattar, professor1,
  11. Jason M R Gill, reader1
    Author affiliations
  1. Correspondence to: J M R Gill
  • Accepted 16 March 2017


Objective To investigate the association between active commuting and incident cardiovascular disease (CVD), cancer, and all cause mortality.
Design Prospective population based study.
Setting UK Biobank.
Participants 263 450 participants (106 674 (52%) women; mean age 52.6), recruited from 22 sites across the UK. The exposure variable was the mode of transport used (walking, cycling, mixed mode v non-active (car or public transport)) to commute to and from work on a typical day.
Main outcome measures Incident (fatal and non-fatal) CVD and cancer, and deaths from CVD, cancer, or any causes.
Results 2430 participants died (496 were related to CVD and 1126 to cancer) over a median of 5.0 years (interquartile range 4.3-5.5) follow-up. There were 3748 cancer and 1110 CVD events. In maximally adjusted models, commuting by cycle and by mixed mode including cycling were associated with lower risk of all cause mortality (cycling hazard ratio 0.59, 95% confidence interval 0.42 to 0.83, P=0.002; mixed mode cycling 0.76, 0.58 to 1.00, P<0.05), cancer incidence (cycling 0.55, 0.44 to 0.69, P<0.001; mixed mode cycling 0.64, 0.45 to 0.91, P=0.01), and cancer mortality (cycling 0.60, 0.40 to 0.90, P=0.01; mixed mode cycling 0.68, 0.57 to 0.81, P<0.001). Commuting by cycling and walking were associated with a lower risk of CVD incidence (cycling 0.54, 0.33 to 0.88, P=0.01; walking 0.73, 0.54 to 0.99, P=0.04) and CVD mortality (cycling 0.48, 0.25 to 0.92, P=0.03; walking 0.64, 0.45 to 0.91, P=0.01). No statistically significant associations were observed for walking commuting and all cause mortality or cancer outcomes. Mixed mode commuting including walking was not noticeably associated with any of the measured outcomes.
Conclusions Cycle commuting was associated with a lower risk of CVD, cancer, and all cause mortality. Walking commuting was associated with a lower risk of CVD independent of major measured confounding factors. Initiatives to encourage and support active commuting could reduce risk of death and the burden of important chronic conditions.

MIDAS (Modafinil in Debilitating Fatigue After Stroke)

This is the first I've ever heard of anything addressing stroke fatigue. I bet you will have to train your doctor about it.
Andrew Bivard, Thomas Lillicrap, Venkatesh Krishnamurthy, Elizabeth Holliday, John Attia, Heather Pagram, Michael Nilsson, Mark Parsons, Christopher R Levi


Background and Purpose—This study aimed to assess the efficacy of modafinil, a wakefulness-promoting agent in alleviating post-stroke fatigue ≥3 months after stroke. We hypothesized that 200 mg of modafinil daily for 6 weeks would result in reduced symptoms of fatigue compared with placebo.
Methods—This single-center phase 2 trial used a randomized, double-blind, placebo-controlled, crossover design. The key inclusion criterion was a multidimensional fatigue inventory score of ≥60. Patients were randomized to either modafinil or placebo for 6 weeks of therapy, then after a 1 week washout period swapped treatment arms for a second 6 weeks of therapy. The primary outcome was the multidimensional fatigue inventory; secondary outcomes included the Montreal cognitive assessment, the Depression, Anxiety, and Stress Scale (DASS), and the Stroke-Specific Quality of Life (SSQoL) scale. The multidimensional fatigue inventory is a self-administered questionnaire with a range of 0 to 100. Treatment efficacy was assessed using linear regression by estimating within-person, baseline-adjusted differences in mean outcomes after therapy. This trial was registered with the Australian New Zealand Clinical Trials Registry (ACTRN12615000350527).
Results—A total of 232 stroke survivors were screened and 36 were randomized. Participants receiving modafinil reported a significant decrease in fatigue (multidimensional fatigue inventory, −7.38; 95% CI, −21.76 to −2.99; P<0.001) and improved quality of life (SSQoL, 11.81; 95% CI, 2.31 to 21.31; P=0.0148) compared with placebo. Montreal cognitive assessment and DASS were not significantly improved with modafinil therapy during the study period (P>0.05).
Conclusions—Stroke survivors with nonresolving fatigue reported reduced fatigue and improved quality of life after taking 200 mg daily treatment with modafinil.
Clinical Trial Registration—URL: Unique identifier: ACTRN12615000350527.

Dana Foundation Cerebrum Podcast: The Four Pillars of Alzheimer’s Prevention - With Dharma Singh Khalsa, M.D.

You will need this since I'm sure your doctor has no protocol to prevent dementia. You are completely on your own.
You need this solution and soon.
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.

Maybe my ideas here?

Dementia prevention 19 ways

Cerebrum Podcast: The Four Pillars of Alzheimer’s Prevention - With Dharma Singh Khalsa, M.D

This Natural Juice Helps Keep Your Brain Young - Beetroot juice

You'll have to guess what amount to take because your doctor will know absolutely nothing about this. I go for pickled beets instead. Maybe about 3 oz. each evening, no clue if it is doing any good.
This sounds like it might be incredibly important immediately post-stroke.
Older brains can perform like younger ones with this supplement.
A beetroot juice supplement can make older brains perform like younger ones, new research shows.
The supplement was given to older adults just before they worked out.
Professor Jack Rejeski, a study co-author, said:
“We knew, going in, that a number of studies had shown that exercise has positive effects on the brain.
But what we showed in this brief training study of hypertensive older adults was that, as compared to exercise alone, adding a beet root juice supplement to exercise resulted in brain connectivity that closely resembles what you see in younger adults.”
People in the study were over 55, did not exercise and had high blood pressure.
They were given the beetroot supplement an hour before a moderate intensity 50-minute treadmill workout.
The critical ingredient in beetroot is nitrate, which is converted to nitric oxide in the body.
Nitric oxide helps increase blood flow.
Professor Rejeski said:
“Nitric oxide is a really powerful molecule.
It goes to the areas of the body which are hypoxic, or needing oxygen, and the brain is a heavy feeder of oxygen in your body.”
The exercise plus the beets help to deliver more oxygen to the brain, helping to give a boost beyond your years.
The study was published in Journals of Gerontology: Medical Sciences (Petrie et al., 2017).

Johnson & Johnson Official 7 Minute Workout

You need exercise both for losing weight and neurogenesis. Ask your doctor to modify this routine for your inabilities. I can't do jumping jacks, pushups, running in place with high knees, rotations. Our fucking failures of stroke associations should be able to modify these for most stroke survivors, but they won't, I bet they don't even know about this.
Or here:
Or here:
The Johnson & Johnson Official 7 Minute Workout App - YouTube
Apps available for your smartphone.
Actual video showing exercises here:

7-Minute Workout

Differences in muscle activity and temporal step parameters between Lokomat guided walking and treadmill walking in post-stroke hemiparetic patients and healthy walkers

I used the Lokomat and it helped because it forced the spasticity into submission. 11 years later and my spasticity still turns my left foot outward while walking. Fucking spasticity. Get rid of that and I could completely recover in no time.
Journal of NeuroEngineering and Rehabilitation201714:32
DOI: 10.1186/s12984-017-0244-z
Received: 24 December 2016
Accepted: 13 April 2017
Published: 20 April 2017



The Lokomat is a robotic exoskeleton that can be used to train gait function in hemiparetic stroke. To purposefully employ the Lokomat for training, it is important to understand (1) how Lokomat guided walking affects muscle activity following stroke and how these effects differ between patients and healthy walkers, (2) how abnormalities in the muscle activity of patients are modulated through Lokomat guided gait, and (3) how temporal step characteristics of patients were modulated during Lokomat guided walking.


Ten hemiparetic stroke patients (>3 months post-stroke) and ten healthy age-matched controls walked on the treadmill and in the Lokomat (guidance force 50%, no bodyweight support) at matched speeds (0.56 m/s). Electromyography was used to record the activity of Gluteus Medius, Biceps Femoris, Vastus Lateralis, Medial Gastrocnemius and Tibialis Anterior, bilaterally in patients and of the dominant leg in healthy walkers. Pressure sensors placed in the footwear were used to determine relative durations of the first double support and the single support phases.


Overall, Lokomat guided walking was associated with a general lowering of muscle activity compared to treadmill walking, in patients as well as healthy walkers. The nature of these effects differed between groups for specific muscles, in that reductions in patients were larger if muscles were overly active during treadmill walking (unaffected Biceps Femoris and Gluteus Medius, affected Biceps Femoris and Vastus Lateralis), and smaller if activity was already abnormally low (affected Medial Gastrocnemius). Also, Lokomat guided walking was associated with a decrease in asymmetry in the relative duration of the single support phase.


In stroke patients, Lokomat guided walking results in a general reduction of muscle activity, that affects epochs of overactivity and epochs of reduced activity in a similar fashion. These findings should be taken into account when considering the clinical potential of the Lokomat training environment in stroke, and may inform further developments in the design of robotic gait trainers.

Cognitive and mood improvements following acute supplementation with purple grape juice in healthy young adults

It would take a lot to extrapolate this to most stroke survivors, they aren't healthy or young. But the real question to be answered; is red wine even better than grape juice for cognition and mood improvements? Both are sorely needed for stroke survivors, When will followup and an updated diet protocol occur?
European Journal of Nutrition
HaskellRamsay CF, et al. –
In this study, researchers explore the benefit of acute supplementation of purple grape juice in healthy young adults. These outcomes in a small sample of healthy young adults propose that purple grape juice can acutely improve aspects of cognition and mood. No major impacts of juice were seen on memory measures, proposing that these may be less susceptible to manipulation following acute supplementation in healthy young adults. Potential mechanisms underlying these impacts include modulation of cerebral blood flow, glucoregulation and inhibition of monoamine oxidase activity, all of which require further exploration.


  • For this research, they designed a randomised, placebo–controlled, double–blind, counterbalanced–crossover study.
  • This study evaluated the impacts of 230 ml purple grape juice or sugar–matched control in 20 healthy young adults.
  • Computerised measures of episodic memory, working memory, attention and mood were finished at baseline and following a 20–min absorption period.


  • In this study, they observed that the purple grape juice significantly enhanced reaction time on a composite attention measure (p = 0.047) and increased calm ratings (p = 0.046) when compared to placebo.
  • Order impacts likewise showed an enduring positive effect on pre–dose memory reaction time (p = 0.018) and post–dose calm ratings (p = 0.019) when purple grape was consumed first.

Study Links Diet Soda to Stroke, Dementia

How long before your hospital removes this from their soda machines? Or never since they don't read research and don't care to keep up-to-date. Other research back at least 5 years had the same conclusion. So if your hospital still has diet drinks they are appallingly incompetent.

But can't determine causality; some associations diminished with adjustments

  • by
    Staff Writer, MedPage Today

Action Points

  • Note that this observational study found an association between artificially-sweetened beverage intake and stroke and dementia, even after accounting for total caloric intake.
  • This does not necessarily imply causality, however, as multiple other confounders may be present.
Higher consumption of artificially sweetened soft drinks was associated with an increased risk of both stroke and dementia in an analysis of more than 4,000 participants in the Framingham Heart Study Offspring cohort, researchers found.
In the observational study, those who drank at least one artificially-sweetened beverage a day were nearly three times more likely to develop ischemic stroke (HR 2.96, 95% CI 1.26–6.97) and 2.9 times more likely to develop Alzheimer's disease (95% CI 1.18–7.07) over 10 years than those who abstained, Matthew Pase, PhD, of Boston University School of Medicine, and colleagues reported in the American Heart Association's journal Stroke.
However, sugary beverages weren't tied to an increased risk of stroke or dementia -- a finding the authors called "intriguing," and one that could have been due to survival bias.
"It is possible that individuals with high intakes of sugary beverages may have died earlier from other illnesses such as heart disease," Pase told MedPage Today. "It is also worth noting that our sample consumed diet soda more frequently than sugar-sweetened soda and this may contribute to differences in findings between regular and diet soda."
He cautioned that the association between artificially sweetened drinks and stroke and dementia seen in their study does not imply causation -- a point emphasized by Marion Nestle, PhD, professor of nutrition, food studies, and public health at New York University, who wasn't involved in the study.
"Association is not the same as causation, although the survival curves are impressive," Nestle said. "I wish the authors had offered a plausible hypothesis for how artificial sweeteners could be causally related to stroke and dementia."
Several other experts commented on the "controversial but inconclusive" nature of the association.
"The relationship with artificially sweetened beverages was not simple or straightforward," said Keith Fargo, PhD, of the Alzheimer's Association. "When the researchers controlled for other risk factors, particularly cardiovascular risk factors, it explained most of the association between artificially sweetened beverage intake and the development of dementia. This kind of data does not allow us to say that drinking [these] beverages causes dementia, or that cutting down on artificially sweetened beverages will reduce a person's risk for dementia."
Pase and colleagues analyzed data from the Framingham Heart Study Offspring cohort on people over age 45 years for the stroke arm (N=2,888) and people over age 60 years for the dementia arm (N=1,484). Both groups were primarily Caucasian and were just under 50% male.
Beverage intake was quantified using the Harvard semiquantitative food-frequency questionnaire at three points: cohort examinations five (1991–1995), six (1995–1998), and seven (1998–2001). Participants were then followed for more than 10 years to determine development of stroke or dementia.
Notably, data collection did not distinguish between the types of artificial sweeteners used in the beverages.
Pase and colleagues found that higher recent and cumulative intake of artificially sweetened soft drinks was linked to an increased risk of ischemic stroke, all-cause dementia, and Alzheimer's dementia -- even after adjustment for total caloric intake, diet quality, physical activity, and smoking status.
However, the associations between recent and higher cumulative intake of artificially sweetened soft drinks and dementia were no longer significant after additional adjustment for vascular risk factors and diabetes mellitus.
"Because our study was observational, we are unable to determine whether artificially sweetened soft drink intake increased the risk of incident dementia through diabetes mellitus or whether people with diabetes mellitus were simply more likely to consume diet beverages," Pase said.
Pase noted the findings complement their sister study, published in Alzheimer's & Dementia, that found higher consumption of both sugary and diet beverages was associated with smaller brain volumes, a marker of accelerated brain aging.
Also using data from the Framingham Heart Study Offspring cohort, this study found that people who more frequently consumed sugary beverages, including sodas and fruit juices, were more likely to have poorer memory, smaller overall brain volumes, and smaller hippocampal volumes.
The researchers concluded that their studies highlight a need for more research into this area, especially given how often people drink artificially-sweetened beverages.
In an accompanying editorial in Stroke, Ralph Sacco, MD, of the University of Miami Miller School of Medicine, agreed, writing that the findings "encourage further discussion and more research into this question, for even small causal effects would have tremendous effects on public health due to the popularity of both artificially sweetened soft drinks and sugar sweetened soft drinks consumption. Both sugar-sweetened and artificially sweetened soft drinks may be hard on the brain."
"This kind of research is critical for examining and uncovering public health relationships that may eventually lead to actionable recommendations," added Fargo.
Rachel Johnson, PhD, MPH, RD, past chair of the American Heart Association's Nutrition Committee and professor at the University of Vermont, suggested that people stick to water, low-fat milk, or other beverages without added sweeteners until more data are available: "We know that limiting added sugars is an important strategy to support good nutrition and healthy body weights, and until we know more, people should use artificially sweetened drinks cautiously," she said in a statement.
The researchers acknowledged several study limitations, including the observational nature of the data, the absence of ethnic minorities, and the use of a self-reported questionnaire to obtain dietary intake data, which may be subject to recall bias.
"Even if someone is three times as likely to develop stroke or dementia," Pase said, "it is by no means a certain fate."
Pase reported funding from the National Health and Medical Research Council.
The Framingham Heart Study is supported by the National Heart, Lung, and Blood Institute and by grants from the National Institute on Aging and the National Institute of Neurological Disorders and Stroke.
Sacco received a National Institutes of Health grant for the Northern Manhattan Study. Gardener is also funded by the National Institutes of Health for her work on the Northern Manhattan Study.
  • Reviewed by F. Perry Wilson, MD, MSCE Assistant Professor, Section of Nephrology, Yale School of Medicine and Dorothy Caputo, MA, BSN, RN, Nurse Planner

Thursday, April 20, 2017

Effects of one session radial extracorporeal shockwave therapy on post-stroke plantarflexor spasticity: a single-blind clinical trial

Is this other research better?

A single blind, clinical trial to investigate the effects of a single session extracorporeal shock wave therapy on wrist flexor spasticity after stroke 

Jan. 2016 

Evidence for the efficacy and effectiveness of THC-CBD oromucosal spray in symptom management of patients with spasticity due to multiple sclerosis

Dec. 2015

Strengthening a Spastic Muscle. Why the Kerfuffle?

Apparatus for reduction of spasticity in male and female patients having spinal cord injury as well as obtaining semen from males by stimulation of ejaculatory nerves 

S2-3 Improvements in spasticity and motor function using a foot bath for people with chronic hemiparesis following stroke


What does your doctor say? Or is s/he like my doctor who knew nothing and told me nothing? No clue what radial extracorporeal shockwave therapy is.

Effects of one session radial extracorporeal shockwave therapy on post-stroke plantarflexor spasticity: a single-blind clinical trial

Pages 483-490 | Received 25 Aug 2015, Accepted 27 Jan 2016, Published online: 13 Mar 2016

Purpose To examine the effects of radial extracorporeal shockwave therapy (rESWT) on plantarflexor spasticity after stroke. Method Twelve patients with stroke were randomly included for this prospective, single-blind clinical trial. Patients received one rESWT session (0.340 mJ/mm2, 2000 shots) on plantarflexor muscle. The Modified Modified Ashworth Scale (MMAS), H-reflex tests, ankle range of motion (ROM), passive plantarflexor torque (PPFT) and timed up and go test (TUG) were measured at baseline (T0), immediately after treatment (T1) and one hour after the end of the treatment (T2). Results Patients had improved the MMAS scores for both the gastrocnemius and the soleus muscles, active and passive ROM, PPFT and TUG over time after rESWT. For the PPFT, it was greater at high velocity than at low velocity, and there was a significant three-way interaction between time, knee position (extended/flexed) and velocity (low/high). The H-reflex latency had decreased at T1, but there was no significant effect on Hmax/Mmax ratio. Conclusions The rESWT improved plantarflexor spasticity, and the effects sustained for one hour, whereas it was not effective in improving spinal excitability.
  • Implications for Rehabilitation
  • One session radial extracorporeal shock wave therapy (rESWT) is safe and effective in improving post stroke plantarflexor spasticity, ankle active and passive range of motion, passive torque, and walking capability.
  • The spasticity scores improved for both the gastrocnemius and the soleus muscles and persisted one hour after rESWT.
  • The magnitude of resistive plantarflexor passive torque in the knee extended position and high velocity was larger over time suggesting greater gastrocnemius spasticity than soleus.
  • The rESWT had no significant effects on alpha motorneuron excitability.