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, September 17, 2014

The management of spasticity in adults

You will notice they say manage, not cure. Dammit expend some intellectual energy and solve the f*cking problem. Point blank ask your doctor what the hell they are doing to solve the spasticity problem.  Screaming in their faces might be useful.  No spitting though. I don't give a damn for their excuse that nothing is clinically proven to work on spasticity. 
Solve it yourself!
  1. Krishnan Padmakumari Sivaraman Nair, consultant1,
  2. Jonathan Marsden, professor2
    Author affiliations
  1. Correspondence to: K P S Nair

Summary points

  • Spasticity is a frequent and debilitating feature of common neurological conditions such as stroke, multiple sclerosis, and traumatic brain and spinal cord injuries
  • The disorder is often associated with pain and discomfort and increased care needs
  • Spasticity is difficult to manage and requires a collaborative approach involving multiple disciplines
  • The evidence for both drug and non-drug treatments of spasticity is limited
  • More research is required to determine the effectiveness of various treatments of spasticity
Spasticity is a common disorder affecting people with long term neurological conditions such as stroke, multiple sclerosis, and traumatic brain and spinal cord injuries. A systematic review of 24 studies on the epidemiology of leg spasticity reported a prevalence of 28-38% in patients with stroke, 41-66% in patients with multiple sclerosis, and 13% in patients with traumatic brain injury.1
Spasticity varies from a subtle neurological sign to a gross increase in tone causing immobility of joints. The disorder is associated with several complications, including falls, pain, pressure ulcers, infections, and contractures,2 although it is not clear whether these complications are caused by spasticity or co-exist independently.1 Spasticity increases care needs and utilisation of healthcare resources,3 and carers of patients with spasticity are more likely to experience anxiety and depression.4 Some patients may make use of their spasticity to sit, stand, walk, or transfer. Management of spasticity requires a balanced approach, weighing the benefits of treatment against the usefulness of the spasticity. Current interventions to treat spasticity lack a robust evidence base, and guidelines often depend on expert recommendations. This review discusses the assessment and treatment of spasticity in adults.

World Alzheimer Report 2014: Dementia and Risk Reduction

A great stroke association would be producing a stroke report like this every year. We have crap for stroke associations, but they do know how to put out press releases.

World Alzheimer Report 2014: Dementia and Risk Reduction

Tuesday, September 16, 2014

Top ten research priorities relating to life after stroke - Lancet Neurology

This was written in 2012 so send your doctor after the information to see what  the results were. What happened to these priorities? Who worked on them?  The people writing these were still stupid because nothing in here is about preventing these problems in the first place by stopping the neuronal cascade of death. Less damaged neurons means less disability.  Doesn't anybody know about Cause and Effect? We seem to have f*cking idiots everywhere.  And yes, I am not following Dale Carnegies ' How to Win Friends and Influence People'. Damn it all if you are not willing to tackle the hard problems get out of the way and let more driven people do the actual work.
In November, 2011, Alessandro Liberati (1954—2012) called for a redefinition of the academic research agenda.1 Liberati supported initiatives such as the UK-based James Lind Alliance (JLA), which has developed models for bringing patients and health professionals together to identify research priorities.2 The JLA aims to ensure that those who undertake and fund health research are aware of what gaps in knowledge matter most to patients, carers, and health professionals.
Working in collaboration with the JLA, from February, 2009, to November, 2011, we completed a priority setting project that has defined a national research agenda relating to life after stroke.
JLA methods involve four key stages:3 (1) gathering of treatment uncertainties, (2) checking of existing research evidence, (3) interim prioritisation to identify the priorities of relevant individuals and stakeholder groups, and (4) a final consensus meeting to reach agreement on the top ten research priorities. We supplemented standard JLA methods of postal and email surveys with novel strategies to ensure that we enabled equal participation of stroke survivors, carers, and health professionals throughout Scotland. We developed these strategies to address barriers to participation, such as those caused by living in remote geographical locations (Scotland's highland and islands) and stroke-related impairments and disabilities. Strategies included face-to-face visits at stroke support groups and clubs, production of information in several formats (eg, an aphasia-friendly information sheet and audio presentation), and provision of information at key national health professional and stroke meetings.
We collected 548 treatment uncertainties (260 from stroke survivors) which, after checking research evidence, were reduced to 226 unique unanswered research questions. 97 people participated in the interim prioritisation process, leading to the identification of 24 shared top priorities. At a final consensus meeting, a representative group of stroke survivors, carers, and health professionals unanimously agreed their top ten priorities for future research (panel). The webappendix and the JLA website provide additional methodological details.
Top ten research priorities relating to life after stroke
  • What are the best ways to improve cognition after stroke?
  • What are the best ways to help people come to terms with the long-term consequences of stroke?
  • What are the best ways to help people recover from aphasia?
  • What are the best treatments for arm recovery and function, including visual feedback, virtual reality, bilateral training, repetitive task training, imagery or mental practice, splinting, electromechanical and robot-assisted arm training, and botulinum toxin?
  • What are the best ways to treat visual problems after stroke?
  • What are the best ways to manage or prevent fatigue?
  • What are the best treatments to improve balance, gait, and mobility, including physiotherapy, gait rehabilitation, visual and auditory feedback, electrical stimulation, different types of ankle foot orthoses, and electromechanical assisted gait training?
  • How can stroke survivors and families be helped to cope with speech problems?
  • What are the best ways to improve confidence after stroke, including stroke clubs or groups, offering support, one-to-one input, and re-skilling?
  • Are exercise and fitness programmes beneficial at improving function and quality of life and avoiding subsequent stroke?
Seven of the top ten priorities are related to stroke-related impairments, such as cognitive problems, aphasia, mobility problems, vision impairment, fatigue, and lack of fitness. However, also included in the top ten are three questions related to the indirect consequences of stroke, covering the issues of coming to terms with life after stroke, helping stroke survivors and carers to cope with speech problems, and confidence after stroke. Stroke survivors and carers made eloquent and convincing arguments for the importance of these issues, highlighting, for example, that there was little point in addressing stroke-related impairments in communication or mobility if one did not have the confidence to participate in daily or recreational activities.
These priorities relating to life after stroke have been generated through a unique, comprehensive, rigorous, and inclusive process, with equal participation from stroke survivors, carers, and health professionals. Here, the research agenda relating to life after stroke has been defined by people to whom it matters most and should now inform the activities of the stroke research community and research funding bodies.
The authors declare that they have no conflicts of interest. This project was supported by funding provided by the Scottish Governement's National Advisory Committee for Stroke. This project was undertaken by the Nursing Midwifery and Allied Health Professions (NMAHP) Research Unit, which is supported by the Scottish Government Health Directorate's Chief Scientist Office. The work presented here represents the views of the authors and not necessarily those of the funding bodies.

Web Extra Material

Supplementary webappendix
Open file
PDF (183K)

Brains can power up to get around Alzheimer's plaques

This might explain why Bernadette the nun could have a brain full of plaque and still function. And maybe explain the fact that higher blood pressure in the elderly leads to less cognitive decline.
A couple of paragraphs, rest at link.
Jagust found that older people with plaques had increased blood flow – which means stronger activation of that brain area – in the regions of the brain that are usually activated during memory formation, compared with the older people who did not have plaques. The team then analysed whether this extra brain activation might be helping to compensate for the plaques.
And the results were clear. In the case of the older people with beta-amyloid, the more accurate their memory of the picture, the more active their brain had been when they studied the image in the fMRI. "That suggested to us that they were able to ramp up activity to retain more information," says Jagust. "We interpret this as a compensation or plasticity. The older people who didn't have amyloid in the brain did not do it."
This boosting of brain activity seems to be related to the amount of plaques a person had. The more beta-amyloid protein someone had, the more they tended to ramp up their brain activity while memorising the scene. However, this effect tailed off in the people with the greatest amount of plaques. "It suggests this is a transitory phenomenon. Eventually, this sort of compensation becomes lost. And that might be something that happens in the progression to cognitive decline," Jagust says.

The results could also help explain why some people have the plaques without appearing to have dementia. "The fact that brain amyloid is detectable in cognitively normal elderly subjects has been used historically as an argument to support the idea that amyloid may not be as toxic as suggested by experimental studies," says Roger Nitsch, a neuroscientist at the University of Zurich in Switzerland. "This work challenges this view by addressing how elderly subjects can retain normal cognition despite the presence of brain amyloid."

Ireland could free up 24,000 hospital beds by letting stroke patients out early

The bean counters at work again. YOU are going to have to get involved and ask for specific research that proves that this is medically better.

‘early supported discharge’ What a pile of steaming crap. Makes it sound like  a walk in the park.
Another way to free up hospital beds would be to suggest to patients that they don't want to disappoint their doctors by their 'failure to die'.

Comparing the efficacy and safety of Crocus sativus L. with memantine in patients with moderate to severe Alzheimer's disease: A double-blind randomized clinical trial

Memantine  is likely one of those things your doctor should be providing to you post-stroke. But your doctor won't do one f*cking thing to stop the neuronal cascade of death and that allows millions of your neurons to die.
Don't listen to me I'm not medically trained although I do know cause and effect and can analyze stuff quite well.

Memantine Enhances Recovery From Stroke

Study: Even the smallest stroke can damage brain tissue, impair cognitive function

Comparing the efficacy and safety of Crocus sativus L. with memantine in patients with moderate to severe Alzheimer's disease



Moxibustion for stroke rehabilitation

I can't see any use for this unless we are talking about extra sensation caused by the pain this produces.;jsessionid=3D70EFD25291A47E66E1B73978E7FFC1.f04t03?


This is the protocol for a review and there is no abstract. The objectives are as follows:
To evaluate the evidence for or against the effectiveness of moxibustion as an adjunctive or as sole therapy for reducing death and disability after stroke.

Dragon boat racing

This past weekend a friend raced on the local river. It was damned depressing watching something that I would be quite good at and would be perfect for my upper arm rehab.  The only problem is that these boats are for sitting, if you really want power you have to kneel, that way you get your core body muscles involved rather than your weak arms.

Stroke rehabilitation services in New Zealand: a survey of service configuration, capacity and guideline adherence

You will need to contact your doctor and get the actual standards to see if they are useful at all. Only results should be used as a way to rate the stroke units, not processes.
1.  tPA full recovery percent,
2.  30 day death rates,
3.  accurate diagnosis of stroke events,
4.  100% recovery.
Summary We surveyed all New Zealand stroke rehabilitation units in late 2013 and asked
them to describe the set-up of the unit and whether they met NZ Stroke Guideline standards
for stroke rehabilitation. Overall, improvements were noted from the last survey in 2007.

Neuromechanical Factors That Limit Walking Speed in Individuals with Post-Stroke Hemiparesis

I'm sure your doctor/therapist can apply any new information in here to your updated stroke walking protocol.

Individuals, post-stroke, present with an array of changes to the neuromuscular system function such as muscle weakness and abnormal muscle activation patterns. Different combinations of these and other altered body functions result in limitations in functional mobility, such as reduced gait speed and high risk for falls. In this series of studies, I developed a deeper understanding of how neuromechanical factors may limit the fastest speed that an individual post-stroke can reach before they are unable to move any faster without losing balance. I conducted three studies. In the first study, my results showed that, after stroke, individuals have the capacity to walk at faster speeds than their overground self-selected maximum walking speed, while walking on a treadmill and when provided horizontal assistance using a robotic device. In the second study, I showed that non-impaired individuals modulated the amplitude and phasing of muscle activity according to the requirements brought about by the existence of horizontal assistive forces during walking at progressively faster speeds. Finally, in the third study I showed that individuals post-stroke also were able to modulate amplitude and phasing of muscle activity in both legs, according to the requirements brought about by the existence of horizontal assistive forces during walking at progressively faster speeds. However, the paretic leg was more responsive to horizontal assistive forces than the non-paretic leg. The understanding gained through these studies provide novel insights regarding the capabilities of individuals with post-stroke hemiparesis to adapt their existing impaired neuromuscular mechanisms into more challenging walking tasks. Each study leads to ideas for the development of potentially more effective rehabilitation protocols targeted at the modulation of amplitude and phasing of muscle activity in order to safely achieve faster walking speeds.
AdviserDavid A. Brown
Source TypeDissertation
SubjectsNeurosciences; Physical therapy; Biomechanics
Publication Number3626475

Sunday, September 14, 2014

1 million views of this blog

I started this back in August, 2010. My first post was  
What my doctor should have told me about stroke recovery
I started out arrogant and progressively became more so and angrier and angrier. Something Peter Levine said to me catalyzed the need to start blogging. At first I thought the answers on recovery were out there somewhere and all I needed to do was to find and publish them. I spent years on stroke forums and never really found any answers and what I wanted to ask about nobody knew the answers. It quickly became obvious there are no answers to stroke recovery. The blog morphed into pointing out  all the research that currently exists and if we had a strategy to follow up on that research and make it translational we could save trillions of neurons each day and massively reduce disability from stroke.. I have not succeeded in getting any changes to the medical stroke world. But I have just begun to fight.

I started out with 10-20 posts a month, now it is a bad month if I don't post at least 150.  I think my best day was 25 posts.

I look at three different ways to influence and change the stroke medical world.
1. Create and be recognized as the thought leader of that great stroke association. Top down.
2. Give the information needed to survivors to push their doctors to create translational research. Bottom up. With 10 million survivors worldwide each year the voices from here could be deafening and promote massive change quickly.
3. Have the stroke doctors influence their organizations (ASA,NSA,WSO) to research and solve all the problems. This is not worth trying anymore, a complete failure for the past 40 years.
The first two are valid and I'm working on both at the same time.

Important posts you should know about:
Stroke risk reduction ideas

13 reasons for marijuana with stroke

Dementia prevention 19 ways 

17 stroke diagnosis possibilities

31 hyperacute - first week possibilities 


Half of all stroke victims could have recovered better if they were placed on community rehab programmes - Ireland

I'm sure 100% of stroke survivors could recover better if we just had our stroke medical teams look at existing research and apply it. But that won't ever occur because everything in stroke is somebody else's problem.

Association between stroke and Alzheimer's disease: Systematic review and meta-analysis

I have been using this study.
Your 33% dementia chance post-stroke from an Australian study
This newest one just says there is a risk but doesn't seem to quantify it.
Regardless, What is your doctor doing to prevent that dementia?
My ideas here;
Dementia prevention 19 ways

Association between stroke and Alzheimer's disease: Systematic review and meta-analysis
The authors conduct a systematic review, to find out the association between stroke and Alzheimer's Disease (AD). These results confirm that AD and intracerebral hemorrhage (ICH) may have common pathogenesis and share preventive treatment measures.
  • The authors conducted this systematic review and meta-analysis of stroke on risk for AD and AD on risk for stroke subtypes to clarify the relation between these two disorders on the basis of the studies published from 1975 to November 2013 in the PubMed, EMBASE, and Cochrane Library databases.
  • In total, 7 cohort studies and 2 nested case-control studies met the inclusion criteria for meta-analysis.
  • For stroke, the pooled effect size for AD risk was 1.59 (95% CI 1.25–2.02; z=3.76; p=0.000).
  • For AD dementia, it was not associated with risk of all strokes or ischemic stroke (IS), but the risk of intracerebral hemorrhage (ICH was higher among persons with AD.
  • The pooled RR for AD in relation to incident IS did not indicate a significant association (RR: 1.13; 95% CI 0.75–1.70; z=0.58; p=0.565).
  • The pooled effect size for AD and ICH risk was 1.41 (95% CI 1.21–1.66; z=4.27; p<0.001).
  • Stroke significantly and independently increased risk for AD and in turn AD increased risk for ICH.

Low testosterone and the risk of dementia in elderly men

Something for your doctor to consider when trying to prevent your 33% dementia chance post-stroke from an Australian study.
  In this study, the authors aim was to examine the association of plasma estradiol and testosterone with risk for dementia in elderly men. Low levels of testosterone are associated with a risk for dementia in elderly men. The association between low bio–T and dementia may be more relevant to men 80 years or older and men with a high level of education.
  • Within the population based Three-City study, including 3650 men age 65 years and older, a case–cohort design was set up after 4-years of follow-up.
  • Baseline plasma levels of total 17-β estradiol (Total-E2), total testosterone (total-T) and bioavailable testosterone (bio-T) were measured for all cases of incident dementia (n=105) and for a random sample of the cohort (n=413).
  • Cox regression models were used to estimate multivariate steroid sex hormone-associated hazard ratios (HR) and 95% confidence intervals of dementia.
  • There was a reverse J-shaped relationship between total-T and risk for dementia (P=.007).
  • Compared with the median tertile, the HRs associated with total-T in the lower and upper tertile were increased (HR, 2.33; P=.026; HR, 1.9, P=.126; respectively).
  • Low bio-T was associated with a greater risk for dementia (HR for one standard deviation of decreasing log(bio-T), 1.29; 95% confidence interval, 1.03–1.62).
  • An interaction was found between bio-T and age (P<.0001), and bio-T and education (P=.044).
  • Risk for dementia associated with low bio-T was greater in older men (80 years or older) than in younger men (younger than 80 years; HR, 3.11; P=.011 vs. HR, 1.07, P=.715, respectively) and in men with high level of education compared with those with low level of education (HR, 2.32; P=.0002 vs. HR, 0.95; P=.790, respectively).
  • No significant association was found between Total-E2 and dementia.

Saturday, September 13, 2014

Korean Factory Workers Don Exoskeletons for Superhuman Strength

I'm sure with a little prodding from a great stroke association that these could be repurposed for stroke. It is only a 10 million person market each year. Carrying stuff one-handed makes me list to one side.
Robotic exoskeletons allow shipyard workers to lift heavy loads with ease. (Courtesy: Daewoo)

What Do Baked Potatoes Have To Do With Stroke?

Potassium. And I bet your hospital does not have a diet high in potassium. Other than orange juice and milk there was not a single item from here in my hospital foods. And just how incompetent is your stroke hospital? That's a question for your hospital president
Selected paragraphs.
An even larger analysis, published last year in the British Medical Journal, found a similar effect: A higher potassium intake decreased stroke risk by 24 percent in people with high blood pressure. All that was needed was an extra two to three servings of fruits or vegetables a day.
In the Swedish study, researchers found that stroke risk decreased as people’s reported potassium intake went up. For every 1,000 mg. increase in daily potassium, the odds of suffering a stroke in the next five to 14 years dropped by 11 percent.
Here are some potassium-rich foods:
Acorn squash, cooked, 1 cup: 896 mg.
Baked potato with skin: 844 mg.
Spinach, cooked, 1 cup: 838 mg.
Lentils, cooked, 1 cup: 731 mg.
Kidney beans, cooked, 1 cup: 713 mg.
Split peas, cooked, 1 cup: 710 mg.
Sweet potato, baked: 694 mg.
Butternut squash, cooked, 1 cup: 583 mg.
Raisins, 1/2 cup: 553 mg.
Avocado, 3 ounces: 540 mg.
Yogurt, low-fat, plain, 1 cup: 531 mg.
Halibut, cooked, 3 ounces: 490 mg.
Banana, medium: 451 mg.
Cantaloupe, 1/4 : 412 mg.
Rainbow trout, farmed, cooked, 3 ounces: 382 mg.
Orange juice, 3/4 cup: 355 mg.
Milk, low-fat, 1 cup: 348 mg.
Broccoli, cooked, 1 cup: 332 mg.

Assessment of movement quality in robot- assisted upper limb rehabilitation after stroke: a review

This is mainly for your therapist but you can look at table 2 on page 8 which lists a whole bunch of upper limb robots, some I haven't even heard of. This is rather appalling that robot rehabilitation is being used with no knowledge of the best way to apply it. Once again stroke survivors are guinea pigs.
Corresponding author
Sheng Quan Xie

Burkhard Wünsche

Department of Mechanical Engineering, The University of Auckland, 2
0 Symonds Street,
Auckland, New Zealand

Department of Computer Science, The University of Auckland, 23 Symond
s Street,
Auckland, New Zealand

Faculty of Electrical Engineering, Universiti Teknikal Malaysia Melaka,
Hang Tuah Jaya,
Melaka, Malaysia
State Key Laboratory of Digital Equipment and Technology, Huazhong Un
iversity of
Science & Technology, Wuhan, China

Studies of stroke patients undergoing robot-assisted rehabilitation have re
vealed various kinematic parameters describing movement quality of the upper limb. However, due to the different level of stroke impairment and different assessment criteria and interventions, the evaluation of the
effectiveness of rehabilitation program is undermined.This paper prese
nts a systematic review of kinematic assessments of movement quality of the upper limb and identifies the suitable parameters describing impairments in stroke patients. A total of 41 different clinical and pilot studies on different phases of stroke recovery utilizing kinematic parameters are evaluated. Kinematic parameters describing movement accuracy are mostly reported for chronic patients with statistically significant outcomes and correlate strongly with clinical assessments. Meanwhile, parameters describing feed-forward sensorimotor control are the most frequently reported in studies on sub-acute patients
with significant outcomes albeit without correlation to any clinical assessments. However, lack of measures in coordinated movement and proximal component of upper limb enunciate the difficulties to distinguish the exploitation of joint redundancies exhibited by stroke patients in completing the movement. A further study on overall measures of coordinated movement is recommended.

Changing a flat tire

Last night after going for a walk to check the skies for northern lights, which was a failure due to clouds and rain. I decided I needed to return a library DVD. Taking the usual route I only got two blocks away and was preparing for a left turn. In the dark and rain I misjudged when the turn lane was coming up. Plowed up and over a curb, flattening the tire and denting the rim.  Luckily I waited until morning to change the tire and put on the donut. It required lots of kneeling and half turns on the two-handed crank which I managed to do by kneeling on the crank and pulling up with my good hand. That took 20 minutes. By that time my left leg was completely shaking. One handed lifting of a tire requires a knee to get it into the back of the hatchback. The new rim won't be available until Tues. and will cost $160.

Brain Trauma to Affect One in Three Players, N.F.L. Agrees

Does no one ever read any research at all? Or even think a little bit?
Maybe by rubbing two functioning neurons together they might look at these.  What's the downside? Fish breath?
Looking at pretreatment with fish oil or post-treatment with fish oil

After the fact here;
Aspirin plus fish oil for a hyperacute treatment
or interventions after the concussions.

Dietary Strategy to Repair Plasma Membrane After Brain Trauma Implications for Plasticity and Cognition

Impairment of paravascular clearance pathways in the aging brain

Another possible reason for your cognitive decline. Has your doctor ruled out the more obscure ones or just used Occams razor to point to your stroke as the cause.?
  1. Benjamin T. Kress1,†,
  2. Jeffrey J. Iliff1,2,3,†,*,
  3. Maosheng Xia1,4,
  4. Minghuan Wang1,
  5. Helen Wei1,
  6. Douglas Zeppenfeld2,
  7. Lulu Xie1,
  8. Hongyi Kang1,
  9. Qiwu Xu1,
  10. Jason Liew1,
  11. Benjamin A. Plog1,
  12. Fengfei Ding1,2,
  13. Rashid Deane1 and
  14. Maiken Nedergaard1,*
DOI: 10.1002/ana.24271


Objective: In the brain, protein waste removal is partly performed by paravascular pathways that facilitate convective exchange of water and soluble contents between cerebrospinal and interstitial fluids. Several lines of evidence suggest that bulk flow drainage via the glymphatic system is driven by cerebrovascular pulsation, and is dependent on astroglial water channels that line paravascular cerebrospinal fluid (CSF) pathways. The Objective of this study was to evaluate whether the efficiency of CSF-ISF exchange and interstitial solute clearance is impaired in the aging brain.
Methods: CSF-ISF exchange was evaluated by in vivo and ex vivo fluorescence microscopy while interstitial solute clearance was evaluated by radio-tracer clearance assays in young (2-3 month), middle age (10-12 month) and old (18-20 month) wild type mice. The relationship between age-related changes in the expression of the astrocytic water channel aquaporin-4 (AQP4) and changes in glymphatic pathway function were evaluated by immunofluorescence.
Results: Advancing age was associated with a dramatic decline in the efficiency of exchange between the subarachnoid CSF and the brain parenchyma. Relative to the young, clearance of intraparechamally injected amyloid β was impaired by 40% in the old mice. A 27% reduction in the vessel wall pulsatility of intracortical arterioles and widespread loss of perivascular AQP4 polarization along the penetrating arteries accompanied the decline in CSF-ISF exchange.
Interpretation: We propose that impaired glymphatic clearance contributes to cognitive decline among the elderly and may represent a novel therapeutic target for the treatment of neurodegenerative diseases associated with accumulation of mis-folded protein aggregates.
Get PDF (2211K)

It Ain't Necessarily So: Why Much of the Medical Literature Is Wrong

I can't always distinguish good vs. bad research, that's why I need a medical person smarter than me that can analyze papers. I'm sure your neurologist isn't any better than me at it, but I doubt s/he has hired an analyst to keep them up-to-date on the latest research. Easy question to find out. 'What are the 10 most important research findings on stroke in the last 10 years? That you are using for your stroke patients?'
In 1897, eight-year-old Virginia O'Hanlon wrote to the New York Sun to ask, "Is there a Santa Claus?"[1] Virginia's father, Dr. Phillip O'Hanlon, suggested that course of action because "if you see it in the Sun, it's so." Today many clinicians and health professionals may share the same faith in the printed word and assume that if it says it in the New England Journal of Medicine (NEJM) or JAMA or The Lancet, then it's so.
Putting the existence of Santa Claus aside, John Ioannidis[2] and others have argued that much of the medical literature is prone to bias and is, in fact, wrong.
Given a statistical association between X and Y, most people make the assumption that X caused Y. However, we can easily come up with 5 other scenarios to explain the same situation.

5 more pages at the link.

Conservative Management vs Intervention for Unruptured Brain Arteriovenous Malformations

For your next discussion with your neurologist.
Behind a paywall, but you can see the first page.

To the Editor Management of brain arteriovenous malformations (bAVMs) has been debated in the recent medical literature. If left untreated, bAVMs confer a risk of neurological morbidity and mortality; however, treatment is associated with risks but offers the potential for lifetime eradication.
Dr Al-Shahi Salman and colleagues1 prospectively followed up 204 patients with unruptured bAVMs over 12 years. Morbidity and mortality rates among patients managed conservatively vs those who underwent interventions (surgical resection, endovascular treatment, radiosurgery, or multimodal intervention) were compared. Over a 4-year period, the authors reported 36 events leading to sustained disability or death in the conservative management group vs 39 in the intervention group. The number of bAVM-associated symptomatic strokes or deaths in patients managed conservatively vs with an intervention was 14 vs 38, respectively.

Friday, September 12, 2014

Regulating nitric oxide production

Which way does your doctor recommend you get your nitric oxide?
Does your doctor even know the benefits of nitric oxide for stroke?

Modulation of Adult Neurogenesis by the Nitric Oxide System

Efficacy of Nitric Oxide in Stroke' (ENOS) study 

Inhaled Nitric Oxide Protects Males But not Females from Neonatal Mouse Hypoxia–Ischemia Brain Injury 


  Inhaled Nitric Oxide Protects Males But not Females from Neonatal Mouse Hypoxia–Ischemia Brain Injury


  Regulation of Injury-Induced Neurogenesis by Nitric Oxide


 Nitric Oxide and the Biological Cascades Underlying Increased Neurogenesis, Enhanced Learning Ability, and Academic Ability as an Effect of Increased Bouts of Physical Activity

  Inhalation of nitric oxide could help improve blood flow to ischemic brain

  Nitric oxide-induced calcium release via ryanodine receptors regulates neuronal function


  Cerebrovascular protection by various nitric oxide donors in rats after experimental stroke


Nitric oxide-induced calcium release via ryanodine receptors regulates neuronal function

 And the latest here:
Blood vessels relax and enable increased blood flow when the enzyme eNOS produces nitric oxide (NO) in the endothelial cells lining the vessels. The activity of eNOS varies with modifications to specific sites in the enzyme, such as S-sulfhydration, a process that is triggered by the gas hydrogen sulfide (H2S). Altaany et al. found that S-sulfhydration of eNOS increased its activity by affecting other modifications to the enzyme. Endothelial cells from mice that could not produce H2S also produced less NO than those from normal mice. Enhancing the S-sulfhydration of eNOS may be an effective strategy to increase blood flow in patients.
Sci. Signal. 7, ra87 (2014).

The MusicGlove: Effective rehabilitation at your fingertips

The starting point requirements seems to be some volitional individual finger movement. That leaves out me.
I think the PossessedHand would be better.
Or maybe the Mozart glove?

A bottle of wine a day is not bad for you and abstaining is worse than drinking, scientist claims

I can grasp any straw to justify my wine and beer consumption. What does your doctor have to say to rebut this? And only accept documented research, not this general crap that alcohol is not good for you.
The recommended daily allowance for alcohol consumption in Britain may well be around the size of a medium to large glass of wine depending on your gender, but a leading scientist in the field has claimed drinking just over a bottle a day would do no harm to your health.

Practice makes perfect — or does it?

You really will need to screw with your therapists mind and deliberately fail in your exercises because that will allow you to learn faster. Practice falling, that will do the job. You will need to ask your doctor if this error memory part of your brain was damaged in your stroke. They will sputter and deflect and not answer the question.
How do we learn from past errors? Herzfeld et al. found that when we practice a movement, the human brain has a memory for errors that is then used to learn faster in new conditions. This memory for error exists in parallel with motor memory's two traditional forms: memory of actions and memory of external perturbations. They also proposed a mathematical model for learning from errors. This model explained previous experimental results and predicted other major findings that they later verified experimentally.
Science, this issue p. 1349

Stroke care at Galloway Community Hospital outperforming national standards - Scotland

This is actually f*cking appalling that the national standards are that low that meaningless stuff is measured. You want to measure;
1.  tPA full recovery percent,
2.  30 day death rates,
3.  accurate diagnosis of stroke events,
4.  100% recovery.
None of this namby-pamby crap.
And unless YOU call them on the carpet, they will continue down this failed path.
The Stranraer hospital has admitted 100 per cent of patients with a stroke to a stroke unit within one day of admission. (SO WHAT?)
These excellent statistics have recently been published by the Stroke Association. The GCH also ranks 12th out of 32 hospitals in meeting stroke care performance standards.
A spokesperson for the organisation said: “This is very good given the positive outcomes that being in a stroke unit can bring. The hospital has also done well with the other standards apart from the time to treat eligible patients with aspirin which is sitting at 79 per cent versus 100 per cent. It is hoped there will be continuous improvement in meeting or outperforming the standards in the future.
“The Scottish Stroke Care Audit Report looks at the quality of stroke care against a set of standards. These standards are mainly around getting diagnosed and treated in the right place, by the right people and at the right time. (Notice that they don't talk about results)

More at link.

Thursday, September 11, 2014

Woman in her twenties discovers that she was born without a cerebellum

Don't be surprised if your insurance informs you that your cerebullar stroke doesn't need any paid for therapy. After all this woman functions quite well without one.

Type AB Blood? You May Be More Prone to Memory Loss

So is your doctor a shoot from the hip person and immediately ascribes your memory loss post-stroke to the stroke? Ask about the bias of Occams' razor and whether or not another reason might be the cause. You will need to force your doctor to think outside the box. At least I'm O negative.
Article here:

Research here:
ABO blood type, factor VIII, and incident cognitive impairment in the REGARDS cohort
  1. Mary Cushman, MD, MSc
  1. Correspondence to Dr. Cushman:
  1. Neurology 10.1212/WNL.0000000000000844


Objective: To assess the relationships among ABO group, factor VIII (FVIII), and incident cognitive impairment in a large, prospective cohort study of black and white adults in the United States using a nested case-control design.
Methods: Incident cognitive impairment was defined using cognitive domain tests over a mean follow-up of 3.4 years. ABO blood group was measured by genotyping in a nested case-control sample of 495 cases with cognitive impairment and 587 controls.
Results: Those with blood group AB and those with higher FVIII had an increased risk of cognitive impairment, adjusting for age, race, region, and sex (respective odds ratios 1.82, 95% confidence interval [CI] 1.15–2.90; and 1.24, 95% CI 1.10–1.38 for 40 IU/dL higher FVIII). Mean FVIII was higher in those with blood type AB (142 IU/dL; 95% CI 119–165) compared with O (104 IU/dL; 95% CI 101–107), and FVIII mediated 18% of the association between AB group and incident cognitive impairment (95% CI for mediation −30% to 68%).
Conclusions: Blood group AB and higher FVIII were associated with increased incidence of cognitive impairment in this prospective study. The association of blood group AB with incident cognitive impairment was not significantly mediated by FVIII levels.

Neuroprotection for ischaemic stroke: Current status and challenges

Boring title - neuroprotection. It gives no sense of urgency. However if you told your doctor that the neuronal cascade of death was occurring right now in your brain, then maybe your doctor might consider doing something about it.  And no mention of Dr. Michael Tymianskis' comment. on the 1000+ failed neuroprotection drugs. I'm not going to compare this to my 177 hyperacute therapies. Your doctor should know about all of them and have contacted researchers to test out those possibilities.
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Stroke is the third cause of death worldwide and the main cause of chronic, severe adult disability. We focus on acute ischaemic stroke, which accounts for approximately 80% of all strokes. The current therapy aims at restoring cerebral blood flow within a narrow time window in order to prevent damaging the “penumbra” which surrounds the infarct core. Intravenous thrombolysis remains the fundamental treatment worldwide, though not ideal for various restrictions and complications, limiting to 10% or less the percentage of patients treated within the appropriate time window.
Neuroprotection is an alternative or adjunct approach to thrombolysis, targeting cerebral parenchyma in the acute ischaemic phase. Furthermore, neurorepair attempts to restore neuronal function in the after-stroke phase in those patients (treated or untreated) with significant impairment.
In the past decades, the efficacy and safety of numerous candidate neuroprotective agents were shown in various animal stroke models. However, in clinical trials, promising pre-clinical studies have not been translated into positive outcomes. Our review will analyse the possible reasons for this failure and the new approaches and recommendations to overcome it, as well as novel strategies targeting additional events in ischaemia cascade. The combination of thrombolysis with pharmacological and non-pharmacological neuroprotective approaches has also been tested. Finally, the neurorepair strategy will be described with special emphasis on the role of cell-based therapies and ischaemic conditioning.
Hopefully, the future therapy of ischaemic stroke will encompass a combination of neuroprotection (to stabilise penumbra), thrombolysis, antithrombotics (for secondary prevention) and neurorepair based on cell therapy plus rehabilitation.

Not enough done for stroke patients - New Zealand

This guy is just wrong, the problem is not that there is not enough one-on-one therapy. That is thinking in the status quo, you will never get ahead in life stuck in the past like that. The problem is that it affects stroke survivors very badly. The solution, yet to be found, is to stop the neuronal cascade of death which would result in much less dead and damaged neurons.
Well shit, only 10% get to full recovery, so your one-on-one therapy is still a failure.It may be better than nothing but it is still a failure
My God, the stupidity, it burns.

Investigation of Sox9 ablation on neuroplasticity and recovery after ishcemic stroke

Another research project for our great stroke association to tackle. Unless you really think your neurologist is smart enough to figure out how to accomplish this by themselves.

Bethany Robin Lenore Bass, The University of Western OntarioFollow
Room 447 Medical Science Building


Master of Science


Anatomy and Cell Biology


Dr. Arthur Brown

Delay of Publication



Neuroplasticity is a key factor in post-stroke functional recovery. A chief inhibitor of post-stroke neuroplasticity is the expression of chondroitin sulfate proteoglycans (CSPGs). Recent research has shown that the transcription factor SOX9 is responsible for upregulating the expression of CSPGs in the injured central nervous system. Accordingly, CSPG levels are significantly lower in mice with the Sox9 gene conditionally knocked out. The purpose of this study was to determine how Sox9 ablation affects neuroplasticity and recovery after stroke. Behavioural test results revealed that Sox9 KO mice exhibited significantly improved functional recovery after stroke compared to controls. This correlated with increased contralesional corticofugal plasticity in the Sox9 KO animals, as highlighted by tract tracing studies. An increase in one type of glutamatergic input marker (VGLUT1) was observed at the deafferented red nucleus of the Sox9 KO mice, but not at the denervated the cervical spinal cord ventral horn. Further investigation into the effects of Sox9 ablation on post-stroke neuroplasticity would be beneficial to determine the potential of Sox9 as a therapeutic target.

Recommended Citation

Bass, Bethany Robin Lenore, "Investigation of Sox9 ablation on neuroplasticity and recovery after ishcemic stroke" (2014). University of Western Ontario - Electronic Thesis and Dissertation Repository. Paper 2338.

New Evidence Shows Sleep Apnea Hurts Your Brain

So your doctor should be treating your sleep apnea immediately post-stroke to prevent the weaker blood flow from the disorder. My test in the hospital was a finger oximeter test that they said showed no sleep apnea. Totally false, all they had to do was ask my ex or me.  You are going to have to demand a sleep test since I'm sure your doctor will not have updated this as a stroke protocol for another 30 years. 
You do want to save as many of your neurons as possible? Don't you?
Employing a measure rarely used in sleep apnea studies, researchers at the UCLA School of Nursing have uncovered evidence of what may be damaging the brain in people with the sleep disorder — weaker brain blood flow.
In the study, published in the peer-reviewed journal PLOS ONE, researchers measured blood flow in the brain using a non-invasive MRI procedure: the global blood volume and oxygen dependent (BOLD) signal. This method is usually used to observe brain activity.  Because previous research showed that poor regulation of blood in the brain might be a problem for people with sleep apnea, the researchers used the whole-brain BOLD signal to look at blood flow in individuals with and without obstructive sleep apnea (OSA)
More at link.

Cognitive Stimulation for Portuguese Older Adults With Cognitive Impairment

There has to be something useful in here for your doctor to give you if you are cognitively impaired post-stroke.

A Randomized Controlled Trial of Efficacy, Comparative Duration, Feasibility, and Experiential Relevance

  1. Jorge Alves, MSc1
  2. Filipa Alves-Costa, MSc2
  3. Rosana Magalhães, MSc1
  4. Óscar F. Gonçalves, PhD1,3
  5. Adriana Sampaio, PhD1
  1. 1Neuropsychophysiology Lab, CIPsi, School of Psychology, University of Minho, Braga, Portugal
  2. 2Justice and Violence Applied Research Unit, CIPsi, School of Psychology, University of Minho, Braga, Portugal
  3. 3Department of Counseling and Applied Educational Psychology, Bouvé College of Health Sciences, Northeastern University, Boston, MA, USA
  1. Jorge Alves, MSc, Laboratório de Neuropsicofisiologia, Escola de Psicologia, Universidade do Minho, Campus de Gualtar 4710-057, Braga, Portugal. Email:


Although some studies point to cognitive stimulation as a beneficial therapy for older adults with cognitive impairments, this area of research and practice is still lacking dissemination and is underrepresented in many countries. Moreover, the comparative effects of different intervention durations remain to be established and, besides cognitive effects, pragmatic parameters, such as cost-effectiveness and experiential relevance to participants, are seldom explored. In this work, we present a randomized controlled wait-list trial evaluating 2 different intervention durations (standard = 17 vs brief = 11 sessions) of a cognitive stimulation program developed for older adults with cognitive impairments with or without dementia. 20 participants were randomly assigned to the standard duration intervention program (17 sessions, 1.5 months) or to a wait-list group. At postintervention of the standard intervention group, the wait-list group crossed over to receive the brief intervention program (11 sessions, 1 month). Changes in neuropsychological, functionality, quality of life, and caregiver outcomes were evaluated. Experience during intervention and costs and feasibility were also evaluated. The current cognitive stimulation programs (ie, standard and brief) showed high values of experiential relevance for both intervention durations. High adherence, completion rates, and reasonable costs were found for both formats. Further studies are needed to definitively establish the potential efficacy, optimal duration, cost-effectiveness, and experiential relevance for participants of cognitive intervention approaches.

Clinical Significance in Dementia Research A Review of the Literature

And if there were any f*cking brains at all in the stroke world an article like this on stroke would be written each year. Or maybe we should have this as an assignment for grad students at all the top neurology programs because it won't get done otherwise.
  1. Syed H. Shabbir, BSc1
  2. Amy E. Sanders, MD, MS1
  1. 1Saul R. Korey Department of Neurology, Albert Einstein College of Medicine, Bronx, NY, USA
  1. Amy E. Sanders, MD, MS, Albert Einstein College of Medicine, Louis and Dora Rousso Building, 1165 Morris Park Avenue, Room 311, Bronx, NY 10461, USA. Email:


Clinical research traditionally relies on measures of statistical significance to assess the strength of evidence while less attention is paid to the practical import of the results. The objective of this study was to provide a critical overview of the current approaches to measuring clinical significance in dementia research and to provide suggestions for future research. A systematic search was conducted of Medline and Embase for original, English-language, peer-reviewed articles published before July 2012. A total of 18 articles met the inclusion criteria, of which 13 used multiple approaches to measure clinical significance. In all, 5 articles used expert opinion as anchors; 4 also used distribution-based approaches. In all, 8 articles used Goal Attainment Scaling; 7 of these also relied on clinician-based impressions of change. Another 3 articles used only clinical global impressions of change, 1 article used changes in symptomatology, and another used the value from literature.

White matter matters in major depressive disorder (MDD)

So your doctor should be able to tell from the damage to your white matter if you are likely to get MDD. Good luck with that. I'm sure your doctor has no objective clue to your white matter damage.

When Scientists Give Up - Stroke version

And this is precisely why we need that great stroke association that will get money from foundations to support research into all the major stroke problems out there.  With no strategy in place stroke problems will never be solved and the ASA, NSA and WSO have their heads up their asses in not acknowledging that the existing stroke world is a complete failure. Someday one of the executives will contact me and we'll have an interesting discussion on why my opinion is the correct one. Although we could quibble where their head is located, I'm sure they would prefer in the sand.