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:

Thursday, October 31, 2013

Push for statewide registry on stroke victims - Illinois

This is so stupid that a law would need to be setup for this to occur. Don't doctors and stroke associations have any idea that this should have been started 40 years ago. If you don't have any facts you can't fix the problems.
The incompetent WSO should have set up  a worldwide one decades ago. But no, we don't care about survivors except to pull in donations. Ok, that was a rant, the WSO could prove me wrong if they want to deign to reply to us pitiful stroke survivors.

A Vital Measure: Your Surgeon’s Skill

All this discussion on the skill of surgeons. Where is the comparable reporting of neurologists skill? Or is that an oxymoron? What is your neurologists efficacy? Better than 10%?

Hippocampal neuron receiving excitatory contacts

Micro photography contestant. Dr. Kieran Boyle; University of Glasgow, Institute of Neuroscience and Psychology; Hippocampal neuron receiving excitatory contacts.We should be able to use this to figure out how to duplicate neuroplasticity.

Stroke and Chiropractic Adjustments

This guy is appalling in his willful disregard for facts. I don't have time to unpack all his lies. Maybe he wants to explain how a baby breaks its neck from an adjustment. Or the death by hanging.

Wednesday, October 30, 2013

Increase in Human Brain Power as a Result of Cranial Frill Cooling

I want even more brainpower so I can be an even bigger asshole. Ask your doctor how to acheive this. Tell them you want to be smarter than them, its not very hard. Frills here;

Increase in Human Brain Power as a Result of Cranial Frill Cooling
J. McGuire, A. Toohie and A. Pohl
Department of Physics and Astronomy, University of Leicester. Leicester, LE1 7RH.
Oct 17, 2013.
This paper outlines the efects of having a small cranial crest of frills containing thin blood vessels to aid with cooling of blood from the brain. We have calculated the increase in brain temperature that such a crest would facilitate to be 1.97C which corresponds to an increase in brain power of 83W or 689%. We have commented on the biological implications of this and deduced that in terms of physics this is a viable mechanism.

Where is the progress in Strokeology?

At least cardiology has some progress and people willing to talk about it. In stroke everyone must be too embarassed to even acknowledge that they are working in such a failed field.

Chickenpox Linked To Stroke Risk: Kids 4 Times More Likely To Have Stroke Within 6 Months Of Infection

Well I hope the anti-vaccine people  see this. I managed to miss this risk after I had chickenpox.

Hydrogel implant enables light-based communication with cells inside the body

This is so blasted simple.
1. Find out how neurons recruit neighboring neurons to help with a task.
2. Attach these implants next to the neurons needing help using the technique found in step 1.
3. Turn on the light communication.
4. Ask your doctor why the hell they aren't working on something so simple even an idiot can figure it out.
A Massachusetts General Hospital press release so your doctor has no excuse for not contacting them.
As researchers develop novel therapies based on inducing specific cells to do specific things, getting the right message to the right group of cells at the right time remains a major challenge.  The use of light to communicate with cells has been restricted by its limited ability to pass through tissues.  Now researchers at the Wellman Center for Photomedicine at Massachusetts General Hospital have developed a way to deliver a light signal to specific tissues deep within the body.  They describe their accomplishment in the current issue of Nature Photonics.

"Scientists only began investigating light-activated therapy a few years ago, but it is generating huge interest," says Wellman investigator Seok Hyun (Andy) Yun, PhD, senior author of the study.  "One of the best known example is use of optogenetics – activation or deactivation of brain cells by illumination with different colors of light – to treat brain disorders. But how to deliver light deep within the brain or other tissues has been a common problem.  The implant we have developed may help solve this problem."

Light passing through an optical fiber (left) can either carry in a signal that stimulates the activity of cells embedded in the hydrogel implant or bring back a signal generated by cells responding to something in their environment. (Harvard Bio-Optics Lab/Wellman Center for Photomedicine, Mass. General Hospital)

Called a light-guiding hydrogel, the implant is constructed from a polymer-based scaffolding capable of supporting living cells and contains cells genetically engineered either to carry out a specific activity in response to light or to emit light in response to a particular metabolic signal.  An optical fiber connects the implant to either an external light source or a light detector.

The investigators first determined the properties of the hydrogel scaffolding – including transparency, flexibility and stability – that would be most appropriate for delivering or detecting a light signal.  After determining how many cells could be implanted into the hydrogel without significantly reducing its ability to transmit a light signal, they developed and tested in mice two different systems, both involving implantation of a 4-centimeter hydrogel beneath the animal's skin.

The first system's implants contained cells genetically engineered to express light-emitting green fluorescent protein (GFP) upon contact with a toxin.  After confirming in vitro the hydrogels' response to nanoparticles containing the toxic metal cadmium, the researchers implanted the hydrogels beneath the skin of three groups of mice.  One group was then injected with the cadmium nanoparticles, the second received nanoparticles encased in a polymer shell that shielded cells from the toxin, and the third received a control saline injection.  The implants only produced a GFP-signal in response to the unshielded nanoparticles, indicating their ability to sense a change – in this instance the presence of a toxin – in the cellular environment.

To investigate a possible therapeutic application for the system, the investigators used a hydrogel implant containing cells that respond to blue light by producing glucagon-like peptide-1 (GLP-1), a protein playing an essential role in glucose metabolism.  After the implants were placed under the skin of mice with diabetes, the blue light signal was delivered for 12 hours.  A day and a half later – 48 hours after the implant – the animals that received the light signal had double the level of GLP-1 in their blood, along with significantly better results in a glucose tolerance test, than did implanted mice not treated with light.

"This work combines several existing technologies well known in their respective fields – such as drug delivery, genetic engineering, biomaterial science, and photonics – to build a new implant system that enables the delivery of photomedicine deep in the body," says Yun, an associate professor of Dermatology at Harvard Medical School and director of the Harvard Bio-Optics Lab. "This is the first time anyone has shown the ability to talk optically – by means of light – with cells deep within the body, both to sense the presence of a toxin and to deliver a cell-based therapy."

The researchers add that future studies should investigate how changing the shape and structure of the hydrogel can improve the implant's light-guiding properties, ways to improve the production and delivery of a therapeutic protein, how the immune system would react to long-term implantation and ways to deliver or detect the light signal that would not require passing a fiber through the skin.

Myunghwan Choi, PhD, of the Wellman Center at MGH is lead author of the Nature Photonics article. Additional co-authors are Jin Woo Choi, Sedat Nizamoglu, and Sei Kwang Hahn, PhD, Wellman Center; and Seonghoon Kim, Korea Advanced Institute of Science and Technology.  Support for the study includes National Institutes of Health grant R21 EB013761, National Science Foundation grant ECS-1101947 and Department of Defense grant FA9550-10-1-0537.

Massachusetts General Hospital, founded in 1811, is the original and largest teaching hospital of Harvard Medical School. The MGH conducts the largest hospital-based research program in the United States, with an annual research budget of more than $775 million and major research centers in AIDS, cardiovascular research, cancer, computational and integrative biology, cutaneous biology, human genetics, medical imaging, neurodegenerative disorders, regenerative medicine, reproductive biology, systems biology, transplantation biology and photomedicine.

Media Contacts: Sue McGreevey,, 617 724-2764

The science behind Thomas Südhof's Nobel prize - explaining synapses

From the Stanford School of Medicine  comes this explanation. Every stroke researcher needs to understand this implicitly and use it to come up with a stroke protocol that recovers lost functions due to our strokes. Its a simple assignment but difficult in completion. Ask your doctor how they will use this information for your 100% recovery.

Why Gardening May Save Your Life

Anything will be used to distract from the complete failure of finding a way to stop the neuronal cascade of death.  Incompetent employees use this to stay employed.

Fitness in 40s, 50s Tied to Later Dementia Risk

So maybe I'm not screwed in getting dementia, except my fitness in my 50s was very negatively impacted by my stroke.

Happy, happy, happy

Three things,
I've become a regular IBM employee, get 10 more days of vacation.
Signed off on final divorce papers, just legal filing to go.
I'm going to Italy for two weeks in Feb. with new friends from Mich.

Tuesday, October 29, 2013

A Breathier Oilskin Tot

Anagram for stroke rehabilitation, along with;
A Bearlike Hint Risotto
A Bearlike Thin Risotto
A Bearlike Hist Tortoni
A Bearlike Shit Tortoni
A Bearlike Hits Tortoni
A Bearlike This Tortoni
A Bearlike Hit Tortonis
A Bearlike Shot Introit
A Bearlike Hots Introit
A Bearlike Host Introit
Do your own here;
My name is;
A Reeked Inn
A Reined Ken
A Denier Ken
A Eked Inner
A Kneed Rein
A Kenned Ire
A Kinder Nee
A Dinner Eke
A Dinner Eek
A Diner Keen
A Diner Knee
Uglier Snoot
Signore Lout
Sturgeon Oil
Surgeon Toil
Tongues Roil
Tongue Roils
Tongue Loris
Rogue Tonsil
Rouge Tonsil

Loonier Guts
Looniest Rug

Insole Grout
Lesion Grout
Liners Outgo
Oriole Stung
Lousier Tong
Lustier Goon 

Leg Iron Oust
Leg Iron Outs
Leg Rosin Out
Leg Irons Out

Lie Gnus Root
Lie Guns Root 

World Stroke Day: stroke is common, disabling, and often preventable - Harvard Medical School

Even a Harvard doctor barely knows anything useful. I hope he responds to my comment because he needs educating.
A comment I put in there, we'll see if I get a decent reply.
What would probably make even more sense would be to prevent the neuronal cascade of death in the first week. Less dead and damaged neurons would directly result in better recoveries.  Dr. Michael Tymianski, of the Toronto Western Hospital Research Institute in Canada mentions 1000 failed drugs that worked in rodents but failed in human trials. These probably need to be looked at again since it has now been proven that rodent inflammation is not the same as human inflammation. In my next stroke I have 31 possibilities that I will insist my doctor provide to me. Things like;
 blood pressure cuffs in the ambulance ride

1. Statins.
2. Fish oil.
     either by injection
     or a feeding tube
3.  Leg compressions
4. anti-depressants -  real ones
5. music listening
6. Sensation overload
7. Coffee -
8. CerAxon
9.  Peptide application
10. Action observation
11.  bFGF administered intravenously
12. Viagra -
13.  Training in lucid dreaming.
14.  Eptifibatide
15.  dietary olive leaf extract
16. ebselen - neuroprotective treatment? within 48 hours
17.  diabetes drug linagliptin
18. Etazolate, an α-secretase activator
19.  Glibenclamide - administered intravenously 6, 12, and 24 hours after reperfusion
20.   Paeoniflorin (PF) - PF treatment for 14 days
21.  administration of nontoxic carbon particles
22.  Ibuprofen
23.  Ceria nanoparticles
24.  Head-of-Bed Optimization of Elevation
25.   antibiotic minocycline
26.   neurotransmitter precursor levodopa
27.   Inhalation of nitric oxide
28.  old flu drug amantadine
29.  Melatonin
30.   opiate antagonists
All these have some research already backing them even if they have not been in human clinical trials. Its worth it to my brain to take some chances to save my neurons from dying from glutamate poisoning, excitotoxicity,Capillaries that don't open due to pericytes,  Inflammatory action leaking through the blood brain barrier.

Stroke management plan drawn up - India

This plan was obviously drawn by people who don't understand that current stroke rehab doesn't work and are just going down the failed road of existing guidelines. Maybe if they would work on some of these 177 hyperacute therapies they could stop the neuronal cascade of death and have much less disability to contend with. But they are doctors, they don't listen to people who know more than them.

NIH Funding for Various Research, Condition, and Disease Categories (RCDC)

The detailed report is here;
A blogger discussing brain disorder funding here;
Stroke funding is dropping because we haven't hit the tipping point for stroke. This completely points out why we need a great stroke association that  funds its own research.
Research would be sponsored. Like the Michael J. Fox Foundation decisions on research would be decided quickly.  Myelin Repair and the Alzheimers Association also sponsor research and should be emulated.

Does the Influence of Stroke on Dementia Vary by Different Levels of Prestroke Cognitive Functioning?: A Cohort Study

The last line means I'm screwed. What is your doctor doing to prevent that?

Gulliford M; Stroke (Oct 2013)

BACKGROUND AND PURPOSE The association between stroke and subsequent dementia or Alzheimer disease is well established. What is less understood is the extent to which this association is dependent on prestroke cognitive functioning. The study estimated the occurrence in poststroke dementia as a function of prestroke cognitive status and incident stroke.
METHODS Study data were derived from the English Longitudinal Study of Ageing, a 10-year long prospective cohort study of older adults living in England. Baseline data (2002/2003) were used to group participants into tertiles of cognitive, memory, and executive functioning before an incident stroke. Data from 4 follow-up surveys were used to identify new stroke and poststroke dementia events.
RESULTS The analyses were based on 10 809 participants aged ≥50 years at baseline. High prestroke executive functioning was associated with lower relative risk (RR) of dementia (RR, 0.24; 95% confidence interval, 0.13-0.45; P<0.001). Stroke was associated with increased RR of poststroke dementia (RR, 2.63; 95% confidence interval, 1.80-3.84; P<0.001). The association of stroke with poststroke dementia was greater for participants with higher prestroke executive functioning (interaction term RR, 4.4; 95% confidence interval, 1.35-14.63; P=0.014). For participants with higher executive functioning, the probability of dementia was 0.3% without stroke and 3.1% after stroke, compared with 1.9% and 5.2% for lower executive functioning.
CONCLUSIONS Stroke and prestroke cognition were independently associated with increased probability of poststroke dementia. Stroke results in disproportionate increase in the risk of dementia when premorbid cognitive functioning is high.

Monday, October 28, 2013

After a Stroke, Running a Half-Marathon

I wish there was a more detailed explanation of the deficits and how they were overcome.

Nerve block works for stroke shoulder pain

But is this just disguising the damage being done? Have we even determined if the pain is real or not? I'm sure your doctor reads  every issue of Rheumatology Update and will tell you about this shortly.

Shoulder pain was common following stroke, affecting up to 25% of patients, yet there was no good treatment for post-stroke shoulder pain, Dr Shanahan told Rheumatology Update.
The rheumatologists from Flinders University found neurologists were coming to them for a solution, so they decided to conduct a study into the effectiveness of nerve blocks in these patients.
They randomised 32 patients to receive a nerve block injection, and 32 patients to placebo.
At week one, four and 12 the SSNB group had a mean VAS reduction of »37mm with a 18mm difference between the intervention and control group, albeit with wide confidence intervals (CI 3-29 at 12 weeks).
The number needed to treat with SSNB to reduce one stroke survivor’s pain by 50% at four weeks and 12 weeks was four, the researchers reported.
“Patients will most likely only need one injection, as pain relief tended to last longer than 12 weeks, and most shoulder pain will settle after 12 months,” Dr Michael Shanahan told Rheumatology Update.
But the researchers were not sure why nerve block worked, and they were currently using transcranial nerve stimulation in a bid to understand the mechanism behind its effectiveness, Dr Shanahan said.
They were also looking at the effectiveness of nerve blocks in other types of stroke, frozen shoulder and in motor neurone disease.

Salvianolate increases heat shock protein expression in a cerebral ischemia-reperfusion injury model

Researchers still haven't figured out that you measure objective results rather than the nebulous(were significantly better) crap these ones are doing.
Stroke remains a worldwide health problem. Salvianolate exerts a protective effect in various microcirculatory disturbance-related diseases, but studies of the mechanisms underlying its protective action have mainly focused on the myocardium, whereas little research has been carried out in brain tissue following ischemia-reperfusion. We assessed the neuroprotective effects of salvianolate in a rat model of cerebral ischemia-reperfusion injury induced using the suture method. At onset and 24 and 48 hours after reperfusion, rats were intraperitoneal y injected with salvianolate (18 mg/kg) or saline. Neurological deficit scores at 72 hours showed that the neurological functions of rats that had received salvianolate were significantly better than those of the rats that had received saline. 2,3,5-Triphenyltetrazolium chloride was used to stain cerebral tissue to determine the extent of the infarct area. A significantly smaller infarct area and a significantly lower number of apoptotic cel s were observed after treatment with salvianolate compared with the saline treatment. Expression of heat shock protein 22 and phosphorylated protein kinase B in ischemic brain tissue was significantly greater in rats treated with salvianolate compared with rats treated with saline. Our findings suggest that salvianolate provides neuroprotective effects against cerebral ischemia-reperfusion injury by upregulating heat shock protein 22 and phosphorylated protein kinase B expression.
Author: Jinnan Zhang    Wei Lu    Qiang Lei    Xi Tao    Hong You    Pinghui Xie

Treating cerebral ischemia-reperfusion injuries with salvianolate
Salvianolic acid B, also called salvia magnesium acetate, is a phenolic acid compound composed of three Danshensu units and one molecule of caffeic acid.
Salvianolic acid B exerts strong resistance to oxidative stress and inflammatory reaction, and improves energy metabolism against cerebral ischemia-reperfusion injuries.
Dr. Wei Lu and his team from the Second Xiangya Hospital, Central South University, China found that administration of salvianolate during reperfusion after ischemia appears to attenuate brain tissue damage and inhibit neuronal apoptosis by increasing heat shock protein 22 and phosphorylated protein kinase B expression.
These findings were published in the Neural Regeneration Research (Vol. 8, No. 25, 2013).
Article: "Salvianolate increases heat shock protein expression in a cerebral ischemia-reperfusion injury model" by Jinnan Zhang, Wei Lu, Qiang Lei, Xi Tao, Hong You, Pinghui Xie (Department of Neurology, Second Xiangya Hospital, Central South University, Changsha 410011, Hunan Province, China)
Zhang JN, Lu W, Lei Q, Tao X, You H, Xie PH. Salvianolate increases heat shock protein expression in a cerebral ischemia-reperfusion injury model. Neural Regen Res. 2013;8(25):2327-2335.

Health Dept reaches out to private sector, NGOs to help stroke patients

You know if these people would just use a few of their brain cells they might come up with the correct answer, and its not what they suggest.  You really don't need more OTs and PTs, you need less dead and dying neurons. Solve the neuronal cascade of death and lots of the disability and deaths in the first month go away.
The state Health Department is ever ready to work with the private sector and non-governmental organisations (NGOs) to create more comprehensive community rehabilitation centres and programmes for stroke patients.
Sarawak General Hospital (SGH) neurologist Dr Sim Siew Hung said providing rehabilitation-physiotherapy and occupational therapy (PTOT) for outpatients is one of the most challenging issues due to the increasing cases of stroke patients amid the lifestyle and modernisation faced by the society today.
“Most district hospitals such as those in Lundu, Serian, Bintulu, Miri and Limbang have their own PTOT unit, but the Health Department is looking to improve PTOT teams at all district hospitals in the state.
“Improving manpower and resources are among the issues that SGH is also working on,” Dr Sim told a press conference after the opening of the state-level World Stroke Day at the Batu Kawah Health Clinic here yesterday by Assistant Minister of Public Health Datuk Dr Jerip Susil.
Also present was state Health director Datu Dr Zulkifli Jantan.
Dr Zulkifli agreed with Dr Sim, who is the event’s organising chairperson, on the need to have more rehabilitation centres to help stroke patients.
He said PTOT units were also available in all major heart centres in urban areas.
He suggested another option – establish sub-centres where the administration and management of patients’ rehabilitation activities could be carried out at home. The care providers for these patients, especially family members, need to be trained to conduct such therapy.
Dr Zulkifli noted that the Social Security Organisation (Socso) had introduced a programme relating to occupational rehabilitation to help patients undergoing physical and occupational therapy.
Socso will bear the cost of the therapy for members to aid their return to work.
“Due to the lack of centres, a large part of the therapy process would have to be home based. Stroke rehabilitation and management requires a lot of discipline.”
In his speech earlier, Dr Zulkifli said the main objective in holding the state-level World Stroke Day was to raise public awareness on  stroke, prevention measures, immediate treatment and rehabilitation.
Public forum, interaction session, health education exhibition and video presentation filled up the day’s programme.

Smart neurons: Single neuronal dendrites can perform computations

If our neurons are so damned smart why don't our doctors know how to engage them to get to our 100% recovery? Your doctor needs to answer that question, keep asking until an answer comes, it will take 30 years at best.
When you look at the hands of a clock or the streets on a map, your brain is effortlessly performing computations that tell you about the orientation of these objects. New research by UCL scientists has shown that these computations can be carried out by the microscopic branches of neurons known as dendrites, which are the receiving elements of neurons.
The study, published today (Sunday) in Nature and carried out by researchers based at the Wolfson Institute for Biomedical Research at UCL, the MRC Laboratory for Molecular Biology in Cambridge and the University of North Carolina at Chapel Hill, examined neurons in areas of the mouse brain which are responsible for processing visual input from the eyes. The scientists achieved an important breakthrough: they succeeded in making incredibly challenging electrical and optical recordings directly from the tiny dendrites of neurons in the intact brain while the brain was processing visual information.
These recordings revealed that visual stimulation produces specific electrical signals in the dendrites – bursts of spikes – which are tuned to the properties of the visual stimulus.
The results challenge the widely held view that this kind of computation is achieved only by large numbers of neurons working together, and demonstrate how the basic components of the brain are exceptionally powerful computing devices in their own right.
Senior author Professor Michael Hausser commented: “This work shows that dendrites, long thought to simply ‘funnel’ incoming signals towards the soma, instead play a key role in sorting and interpreting the enormous barrage of inputs received by the neuron. Dendrites thus act as miniature computing devices for detecting and amplifying specific types of input.
“This new property of dendrites adds an important new element to the “toolkit” for computation in the brain. This kind of dendritic processing is likely to be widespread across many brain areas and indeed many different animal species, including humans.”
Funding for this study was provided by the Gatsby Charitable Foundation, the Wellcome Trust, and the European Research Council, as well as the Human Frontier Science Program, the Klingenstein Foundation, Helen Lyng White, the Royal Society, and the Medical Research Council.

Disruption of neurogenesis by hypothalamic inflammation in obesity or aging

So whom is going to do the followup research that determines how much obesity and aging impairs neurogenesis?  Damn I want to know. Demand your doctor follow up and do some actual work that might help your recovery. Or are they all just lazy bastards living off your payments for non-performance and your non-recovery?

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Adult neural stem cells contribute to neurogenesis and plasticity of the brain which is essential for central regulation of systemic homeostasis. Damage to these homeostatic components, depending on locations in the brain, poses threat to impaired neurogenesis, neurodegeneration, cognitive loss and energy imbalance. Recent research has identified brain metabolic inflammation via proinflammatory IκB kinase-β (IKKβ) and its downstream nuclear transcription factor NF-κB pathway as a non-classical linker of metabolic and neurodegenerative disorders. Chronic activation of the pathway results in impairment of energy balance and nutrient metabolism, impediment of neurogenesis, neural stem cell proliferation and differentiation, collectively converging on metabolic and cognitive decline. Hypothalamic IKKβ/NF-κB via inflammatory crosstalk between microglia and neurons has been discovered to direct systemic aging by inhibiting the production of gonadotropin-releasing hormone (GnRH) and inhibition of inflammation or GnRH therapy could revert aging related degenerative symptoms at least in part. This article reviews the crucial role of hypothalamic inflammation in affecting neural stem cells which mediates the neurodegenerative mechanisms of causing metabolic derangements as well as aging-associated disorders or diseases.

Sunday, October 27, 2013

World Stroke Day - Oct. 29

F*cking  Whoopee
Just another day to put out press releases rather than doing the difficult tasks of figuring out how to stop the neuronal cascade of death. That tipping point is still out there for stroke.

This is taken from a American Stroke Association email.

Let's come together on World Stroke Day (Oct. 29) to raise awareness that stroke is largely preventable, treatable and beatable. Stroke is the No. 4 killer in the United States. Each year 15 million people worldwide experience a stroke, which claims a life every six seconds.

Join us Oct. 28 for a Google+ Hangout with AHA/ASA and AARP experts to learn about caring for stroke survivors. Learn more

Largely preventable - Maybe, with the generic admonitions like these   rather than specific ones like these 11 referenced and specific ideas.
Treatable - Completely wrong, the 12% efficacy of tPA and non-treatment of the neuronal cascade of death points to failure to me.
Beatable - Bullsheet, Only 10% fully recover, very poor odds.

Passion in stroke

Our stroke associations and the people working for them  obviously do not have it because if they did everyone of us stroke bloggers would have been contacted numerous times. It's probably just a boring job to them. Then get the hell out of the way for passionate survivors.
The 50 Best Work And Passion Quotes Of All Time
 The 50 Best Work And Passion Quotes Of All Time
40 Quotes to Help You Follow Your Passion
Every great dream begins with a dreamer. Always remember, you have within you the strength, the patience, and the passion to reach for the stars to change the world.
Harriet Tubman
There is no passion to be found playing small - in settling for a life that is less than the one you are capable of living.
Nelson Mandela

The 50 Best Work And Passion Quotes Of All Time
The 50 Best Work And Passion Quotes Of All Time
The 50 Best Work And Passion Quotes Of All Time
The 50 Best Work And Passion Quotes Of All Time
The 50 Best Work And Passion Quotes Of All Time

Make no little plans

If we are going to solve stroke this quote from Daniel Burnham
American architect (1846 – 1912)

American architect (1846 – 1912)

“Make no little plans. They have no magic to stir men's blood and probably themselves will not be realized. Make big plans; aim high in hope and work, remembering that a noble, logical diagram once recorded will never die, but long after we are gone will be a living thing, asserting itself with ever-growing insistency.” 
Of course right now there are no plans at all. Damn them all to hell. We need our great stroke association because everything else is a failure.
Big plans will drive optimism and money.

Saturday, October 26, 2013

Poetry readings

Friends set up one of these this weekend. I got to practice talking out loud.
Mine were the Cremation of Sam McGee by Robert Service
and     Counting Moles by Hafiz the great Sufi master

Don't tell all of their

      They might
Count each others moles
That reside in the shy

They keep that tally strictly
       To themselves.

          God and I
    Have signed a contract
To be even more intimate than

Though a clause

Something about not drawing detailed maps
          To all His beautiful


Stroke Director of Hard Truths

I got this  idea from a fundraising appeal. If we don't set goals we will never get anywhere.
1.  The hard truth is that the stroke medical world doesn't really care if we get better or not. They get paid regardless of how well we recover. 
2.  The existing stroke associations don't care either because the more disabled we are the more likely we will be pitied and thus can be used to pull in more donations.
3.  Researchers don't care about us. They are just into finding the next interesting project that will pull in funding money for their lab.
4.  We are completely on our own and the sooner we realize that the better off we we will be.
I am being an agent provocateur here but someone has to be the asshole that points out that no one is going to do a thing for you unless there is a payoff back to them.

Common BP Drugs Tied to Lower Risk of Alzheimer's

Ask your doctor if this 50% reduction is enough to offset your 33% chance of developing Dementia/Alzheimers after a stroke.?  
It should be damn easy for your doctor to find out, look at the bolded study leader, if s/he can't pick up the phone and find that person you have a  doctor to fire.
Although it remains unclear exactly how drugs such as ACE inhibitors or diuretics might protect the brain, researchers say these new findings could lead to a better understanding of Alzheimer's and new treatments to slow or delay the progression of the memory-robbing disease.
"We found a risk reduction by 50 percent. That tells you there must be something there," said study leader Dr. Sevil Yasar, an assistant professor of medicine in the department of geriatric medicine and gerontology at the Johns Hopkins University School of Medicine.

Nano-dwarves turn tumor assassins

And if we had anyone with brains at all we would be studying this for drug delivery for those neuroprotective drugs we still have to find.

Important step towards stem cell-based treatment for stroke

Good news but someone is going to have to do a human clinical trial. Who will take on that challenge? ASA, NSA, WSO? Don't make me barf.

Hands-free ultrasound device with clot-busting drug safe for stroke patients

But have they even considered and checked that they just have moved the damage down to smaller arteries? I compare it to an asteroid approaching earth and we send out some type of explosive device to blow it up. Unless that explosion  pulverizes it enough so that the tiny pieces burn up on entry the earth will still be destroyed or major damage will still occur. Will they be checking and scanning the brain afterward to ensure that they didn't just move the problem down to tiny arteries?

Effective Natural Treatment May Help Brain Damage Caused by Stroke

And how long will something as simple as this take to  get rolled out to all stroke hospitals and rehab centers?  50 years?
Research findings just announced at the Canadian Stroke Congress provide hopeful news for stroke victims. A treatment has been documented that can improve memory, language, thinking and judgment problems by almost 50 percent — all within about six months after a person suffers a stroke. The therapy isn’t a new big drug or surgical treatment. Instead, it is simply consistent exercise that triggers healing in the brain.
Forty-one patients, 70 percent of  them with mild to moderate walking problems requiring a cane or walker, took part in a five-day-a-week aerobic and strength/resistance training program that was adapted to their physical limitations.
The workouts included walking, lifting weights and doing squats and were designed to imitate activities most healthy people would do in daily life. The results? At the conclusion of the program, the researchers found “significant improvements” in overall brain function in the participants. Attention, concentration, planning and organizing improved the most. Muscle strength and walking ability improved dramatically, too.
Not only does exercise dramatically improve cognitive abilities following a stroke, but it could also save the lives of many stroke victims. In a media statement, lead researcher Susan Marzolini of the Toronto Rehabilitation Institute pointed out that people who have cognitive deficits after strokes have a threefold risk of dying. They are also far more likely to be institutionalized.
“If we can improve cognition through exercise, which also has many physical benefits, then this should become a standard of care for people following stroke,” Marzolini said. “These results provide compelling evidence that by improving cardiovascular fitness through aerobic exercise and increasing muscle mass with resistance training, people with stroke can improve brain health.”
Exercising to improve physical and mental status after a stroke may not sound like a new idea, but it is actually an approach to rehabilitation that is too often ignored. Marzolini is urging the medical community to give people with stroke-related impairments access to exercise programs. “Modified exercise programs are desperately needed — they can be adapted for people following stroke, and we think they can provide huge health benefits,” she emphasized.
In addition, people who have never had a stroke can up their odds of staying stroke-free by exercising. “Healthy living is important for reducing your risk for stroke, recovering from stroke and preventing another,” Ian Joiner, director of stroke for the Heart and Stroke Foundation, noted in a press statement about the new study. “All of us should manage our risk factors for stroke and, when needed, have access to information and counseling about strategies to modify our lifestyle choices.”
Read more: Natural News

Friday, October 25, 2013

Theranostic Quantum Dots for Crossing Blood-Brain Barrier in vitro and Providing Therapy of HIV-associated Encephalopathy

Blow your doctors mind away and ask when Quantum dots are going to be used to deliver  neuroprotective drugs thru the blood brain barrier. Ask for a detailed explanation of how Schrodingers cat gets reduced in size to a quantum dot.
  • 1 College of Optoelectronic Information Engineering, Shenzhen University, China
  • 2Department of Medicine, Division of Allergy, Immunology and Rheumatology, The State University of New York at Buffalo, USA
  • 3Department of Chemistry, University of Delhi, India
  • 4School of Electrical and Electronic Engineering, Nanyang Technological University, Singapore
The blood-brain barrier (BBB) is a complex physiological checkpoint that restricts the free diffusion of circulating molecules from the blood into the central nervous system (CNS). Delivering of drugs and other active agents across the blood brain barrier (BBB) is one of the major technical challenges faced by scientists and medical practitioners. Therefore, development of novel methodologies to address this challenge holds the key for both the diagnosis and treatment of brain diseases, such as HIV-associated encephalopathy (HIVE). Bioconjugated Quantum dots (QDs) are excellent fluorescent probes and nano-vectors, being designed to transverse across the BBB and visualize drug delivery inside the brain. This paper discusses the use of functionalized quantum dots for crossing the blood brain barrier and treating brain disease. We highlight the guidelines for using in vitro BBB models for brain disease studies. The theranostic QDs offers a strategy to significantly improve the effective dosages of drugs to transverse across the BBB and orientate to the targets inside the brain.

C-reactive protein and cognition are unrelated to leukoaraiosis

My doctor just threw off a comment to me that I had had some earlier infarcts, so I'm assuming it was some white matter hyperintensities, obviously not important since I didn't get to see a picture of them or any explanation of what to do about them. My doctor told me nothing and as far as I could tell knew nothing, did nothing and should have never been paid for his non-efforts. So even though I have leukoaraiosis I think my cognition is still damn good, better than my doctors.
Inflammation has been increasingly recognized as component in cerebrovascular (1) and neurodegenerative diseases (2, 3). In addition, biological aging of the brain is partly attributable to aging of the cerebrovascular circulation and the effects of vascular changes on the brain (4). Inflammation has been linked to the pathogenesis of cardiovascular disease, obesity and insulin resistance, which are so related to cognitive impairment (5). The hypothesis that inflammation is related to cognitive impairment, although new, is consistent (2). Therefore, few studies evaluated that circulating inflammatory proteins are associated with increased risk of dementia (6), cognitive impairment (7) and cerebral white matter lesions (WML), common referred to leukoaraiosis (8-10).
CRP, composed of five 23 kDa subunits, is a hepatically derived pentraxin that has important role in the human immune system (11). That protein is a sensitive nonspecific marker of systemic low-grade inflammation (5) and increased serum concentrations of CRP have been associated with impaired cognition, stroke and depression (2, 6, 8).

Beyond pro-inflammatory response, that causes neuronal damage directly, increased concentrations of CRP acting as cardiovascular risk factor - approved predictor by Food and Drug Administration - or causing brain atherosclerosis can result in cerebral macro or microangiopathies. Both lesions can disrupt the integrity of frontal-subcortical circuits and are responsible for the development of cognitive impairment, dementia or depressive disorders (12). There are some evidences that elevated serum CRP levels may be a useful biomarker to identify individuals at an increased risk for cognitive impairment (7).

Hospitals in GWTG-Stroke program more likely to provide recommended stroke treatment

The stupidity of this statement is that the recommended stroke treatments only have a 10% full recovery rate, and that really has nothing to do with the treatment. They don't do a damn thing about the neuronal cascade of death. Everyone associated with them should be fired for incompetence.

Results people, Results

Proof That Failure Can Lead to Success - Dilbert

Words of wisdom from Scott Adams. We have to believe in failure because we probably have to fail thousands of times before we become successful at rehab. Start failing right now. I guess I'm not very good at failure yet, I have lots to recover yet.

Raising Awareness in Stroke Excellence (RAISE) Awards - National Stroke Association

I guess I didn't win anything, but I hope they were mad at my blog posts.

Keep positive after a stroke!

You know what would really help to keep a positive after a stroke?
Less dead and damaged neurons because your doctors have stopped the neuronal cascade of death.  This just puts all the responsibility for getting better after a stroke on the survivor. Its called blaming the victim. Stop that!

Thursday, October 24, 2013

Experimental drug reduces brain damage in rodents

Clinical trials for humans were supposed to start over a year ago, so ask your doctor what happened.

Carotid Stenting Tied to Higher Stroke Risk in Seniors

Someone mentioned to me that you really don't want inflexible items like stents in your flexible arteries.
Maybe your doctor can tell you about these options;
Watermelon juice reverses hardening of the arteries
Lipitor, Crestor Both Turn Back Plaque 
Statins Tame Plaque Inflammation 
Targeting Arterial Plaque
Take Two Robots and Call Me in the Morning
Infusing Good Cholesterol May Help Unclog Arteries 
High Intensity Focused Ultrasoundtechnology to treat PAD noninvasively.
But I bet your doctor knows about none of these.

Stroke Numbers Up Worldwide

You can read all the depressing statistics at the article. The existing stroke world is totally unprepared for the coming tsunami of strokes.
A couple of select paragraphs.
In 2010, there were 16.9 million people who had a first stroke, 33 million stroke survivors, and 5.9 million people who died from a stroke -- increases of 68%, 84%, and 26% respectively since 1990, according to Valery Feigin, MD, of the Auckland University of Technology in New Zealand, and colleagues.
If those trends continue, there will be an estimated 12 million stroke deaths, 70 million stroke survivors, and more than 200 million DALYs lost globally each year by 2030, with low- and middle-income countries bearing the brunt of the problem, they noted.
Another analysis by Feigin's group published in The Lancet Global Health showed that hemorrhagic -- and not ischemic -- stroke accounted for the majority of the worldwide burden of deaths and disability-adjusted life years lost due to stroke.
 This will mean that objective diagnosis will become even more important and research into bleeders will need to speed up.

Lack of rehabilitation leaves most stroke survivors disabled - China

And yet most acupuncturists point to China and its overwhelming use of acupuncture for strokes as the reason for using that placebo.
The real problem here is not lack of rehabilitation, its the lack of preventing more disability by stopping the neuronal cascade of death.
A LACK of after-surgery rehabilitation has resulted in a high percentage of disability among the 10.36 million stroke survivors over 40 years old in the nation, experts said.
Compared with the 80 percent rehabilitation rate of stroke survivors in Western countries, over 70 percent of Chinese patients who survived stroke were left with disorders like paralysis and serious language deficiencies. About 40 percent of them have very serious disabilities.
Early detection and treatment while a stroke is taking place, effective therapy and rehabilitation afterwards are all keys for patients' survival and recovery.
Stroke patients who receive early and effective rehabilitation training have a three times higher recovery rate than those who don't receive rehabilitation, said Wang Yanni from Pinetree China, a private company that calls itself the nation's first professional facility offering at-home care and service for after-surgery patients or those needing rehabilitation after surviving diseases.
Teamed up with domestic elderly care organizations, Pinetree announced it will offer free rehabilitation for 20,000 after-stroke patients living in Beijing and Shanghai in the following year.

Wednesday, October 23, 2013

Observations From the Heart Saturated fat is not the major issue - BMJ

And what does your doctor think of debunking most of the standard heart-healthy prescriptions?
A Los Angeles Times column about this here;
Time to end the war against saturated fat?

MD Anderson Taps IBM Watson to Power "Moon Shots" Mission Aimed at Ending Cancer, Starting with Leukemia

And if we had anything approaching a great stroke association, the news would be that Dr. Watson would be analyzing all the data out there to prevent and treat strokes. But alas, we have shit for brains.
The University of Texas MD Anderson Cancer Center and IBM (NYSE: IBM) today announced that MD Anderson is using the IBM Watson cognitive computing system for its mission to eradicate cancer. Following a year-long collaboration, IBM and MD Anderson will showcase a prototype of MD Anderson’s Oncology Expert AdvisorTM powered by IBM Watson. The organizations will discuss their shared vision to leverage Watson’s cognitive computing power to help patients by enabling clinicians to uncover valuable insights from the cancer center’s rich patient and research databases.

Pa passes “I’m sorry” law to improve physician-patient communication

So instead of just saying I don't know, the doctors can continue spouting whatever comes out of their mouths and then reply, 'I'm sorry'. What a piece of crap.

Nasal Administration of Recombinant Osteopontin Attenuates Early Brain Injury After Subarachnoid Hemorrhage

Is this research settled enough that it should be rolled out to all hospitals?  What clinical trials are needed?  The Joint Commission should be responsible for something like this but they won't do anything. Its up to you to get it into the hospital you plan on visiting after your next stroke. If only we had a great stroke association that would take care of all these  survivor needs and make sure doctors and hospitals were up-to-date.
  1. John H. Zhang, MD, PhD
+ Author Affiliations
  1. From the Departments of Physiology and Pharmacology (B.C.T., O.A., K.D., P.R.K., J.Y., J.H.Z.) and Neurosurgery (J.H.Z.), Loma Linda University School of Medicine, CA.
  1. Correspondence to John H. Zhang, MD, PhD, Department of Neurosurgery, Loma Linda University, Loma Linda, CA 92534. E-mail


Background and Purpose—Neuronal apoptosis is a key pathological process in subarachnoid hemorrhage (SAH)–induced early brain injury. Given that recombinant osteopontin (rOPN), a promising neuroprotectant, cannot pass through the blood–brain barrier, we aimed to examine whether nasal administration of rOPN prevents neuronal apoptosis after experimental SAH.
Methods—Male Sprague–Dawley rats (n=144) were subjected to the endovascular perforation SAH model. rOPN was administered via the nasal route and neurological scores as well as brain water content were evaluated at 24 and 72 hours after SAH induction. The expressions of cleaved caspase-3, phosphorylated focal adhesion kinase (FAK), and phosphorylated Akt were examined using Western blot analysis. Neuronal cell death was demonstrated with terminal deoxynucleotid transferase-deoxyuridine triphosphate (dUTP) nick end labeling. We also administered FAK inhibitor 14 and phosphatidylinositol 3-kinase inhibitor, Wortmannin, prior to rOPN to establish its neuroprotective mechanism. ELISA was used to measure rOPN delivery into the cerebrospinal fluid.
Results—Cerebrospinal fluid level of rOPN increased after its nasal administration. This was associated with improved neurological scores and reduced brain edema at 24 hours after SAH. rOPN increased phosphorylated FAK and phosphorylated Akt expressions and decreased caspase-3 cleavage, resulting in attenuation of neuronal cell death within the cerebral cortex. These effects were abolished by FAK inhibitor 14 and Wortmannin.
Conclusions—Nasal administration of rOPN decreased neuronal cell death and brain edema and improved the neurological status in SAH rats, possibly through FAK–phosphatidylinositol 3-kinase–Akt–induced inhibition of capase-3 cleavage.

Tuesday, October 22, 2013

Ischemic Stroke Brain Sends Indirect Cell Death Signals to the Heart

And if we had decent causes of death we wouldn't have the catchall of death caused by stroke. That is not detailed enough to be able to figure out how to stop these types of deaths if we don't autopsy them properly. Is your neurologist calling in a cardiac doctor to make sure your heart continues to function ok after your stroke? Damn there is going to be a lot to remember to tell my doctor about keeping me alive after my next stroke.
  1. Cesar V. Borlongan, PhD
+ Author Affiliations
  1. From the Department of Neurosurgery and Brain Repair, University of South Florida College of Medicine, Tampa, FL (H.I., N.T., J.V., Y.K., C.V.B.); Department of Ophthalmology, Hyogo College of Medicine, Nishinomiya, Japan (H.I., O.M.); and Department of Stem Cell Biology and Histology and Department of Anatomy and Anthropology, Tohoku University Graduate School of Medicine, Sendai, Japan (M.D.).
  1. Correspondence to Cesar V. Borlongan, PhD, Department of Neurosurgery and Brain Repair, University of South Florida, 12901 Bruce B. Downs Blvd MDC78, Tampa, FL 33612. E-mail


Background and Purpose—Ischemic stroke is a leading cause of mortality and morbidity in the world and may be associated with cardiac myocyte vulnerability. However, it remains uncertain how an ischemic brain contributes to cardiac alternations. Here, we used experimental stroke models to reveal the pathological effects of the ischemic brain on the heart.
Methods—For the in vitro study, primary rat neuronal cells were subjected to 90-minute oxygen–glucose deprivation (OGD). Two hours after OGD, the supernatant was collected and cryopreserved until further biological assays. Primary rat cardiac myocytes were exposed to ischemic–reperfusion injury and subsequently to the supernatant derived from either the OGD or non–OGD-exposed primary rat neuronal cells for 2, 6, 24, or 48 hours. Thereafter, we measured cell viability and mitochondrial activity in rat cardiac myocytes. For the in vivo study, we subjected adult rats to transient middle cerebral artery occlusion, and their brains and hearts were harvested for immunohistochemical analyses at 3 months later.
Results—The supernatant from the OGD, but not the non–OGD-exposed primary rat neuronal cells, caused significant reduction in cell viability and mitochondrial activity in rat cardiac myocytes. Ischemic stroke animals displayed phenotypic expression of necrosis, apoptosis, and autophagy in their hearts, which paralleled the detection of these same cell death markers in their brains.
Conclusions—Ischemic stroke was accompanied by cardiac myocyte death, indicating a close pathological link between brain and heart. These results suggest a vigilant assessment of the heart condition in stroke patients, likely requiring the need to treat systemic cardiac symptoms after an ischemic brain episode.

How Well Do Standard Stroke Outcome Measures Reflect Quality of Life?

I'm sure our insurance doesn't care about our quality of life. Plateau and get them off of insurance.
  1. Marian Brady, PhD
  2. on behalf of the VISTA Collaboration*
+ Author Affiliations
  1. From the Nursing, Midwifery and Allied Health Professions Research Unit, Glasgow Caledonian University, United Kingdom (M.A., M.B.); and Institute of Cardiovascular and Medical Sciences, University of Glasgow, Western Infirmary, United Kingdom (M.A., R.F., T.Q.).
  1. Correspondence to Myzoon Ali, PhD, Nursing, Midwifery and Allied Health Professions Research Unit, Buchanan House, Glasgow Caledonian University, Glasgow, G4 0B, United Kingdom. E-mail


Background and Purpose—Quality of life (QoL) is important to stroke survivors yet is often recorded as a secondary measure in acute stroke randomized controlled trials. We examined whether commonly used stroke outcome measures captured aspects of QoL.
Methods—We examined primary outcomes by National Institutes of Health Stroke Scale (NIHSS), Barthel Index (BI) and modified Rankin Scale (mRS), and QoL by Stroke Impact Scale (SIS) and European Quality of Life Scale (EQ-5D) from the Virtual International Stroke Trials Archive (VISTA). Using Spearman correlations and logistic regression, we described the relationships between QoL mRS, NIHSS, and BI at 3 months, stratified by respondent (patient or proxy). Using χ2 analyses, we examined the mismatch between good primary outcome (mRS ≤1, NIHSS ≤5, or BI ≥95) but poor QoL, and poor primary outcome (mRS ≥3, NIHSS ≥20, or BI ≤60) but good QoL.
Results—Patient-assessed QoL had a stronger association with mRS (EQ-5D weighted score n=2987, P<0.0001, r=−0.7, r2=0.53; SIS recovery n=2970, P<0.0001, r=−0.71, r2=0.52). Proxy responses had a stronger association with BI (EQ-5D weighted score n=837, P<0.0001, r=0.78, r2=0.63; SIS recovery n=867, P<0.0001, r=0.68, r2=0.48). mRS explained more of the variation in QoL (EQ-5D weighted score=53%, recovery by SIS v3.0=52%) than NIHSS or BI and resulted in fewer mismatches between good primary outcome and poor QoL (P<0.0001, EQ-5D weighted score=8.5%; SIS recovery=10%; SIS-16=4.4%).
Conclusions—The mRS seemed to align closely with stroke survivors’ interests, capturing more information on QoL than either NIHSS or BI. This further supports its recommendation as a primary outcome measure in acute stroke randomized controlled trials.

Suprascapular Nerve Block for Shoulder Pain in the First Year After Stroke

Is this a possibility for helping your recovery along? You will need to bring it up to your doctors because they won't know about it.
  1. E. Michael Shanahan, PhD
+ Author Affiliations
  1. From the Department of Rehabilitation and Aged Care (Z.A.-W., M.C.) and Department of Rheumatology (E.M.S.), Flinders University, Daw Park, South Australia.
  1. Correspondence to Zoe Adey-Wakeling, BMBS, Department of Rehabilitation and Aged Care, C Block, Repatriation General Hospital, Daws Road, Daw Park SA 5041. E-mail


Background and Purpose—Shoulder pain is a common complication after stroke that can impede participation in rehabilitation and has been associated with poorer outcomes. Evidence-based treatments for hemiplegic shoulder pain are limited. Suprascapular nerve block (SSNB) is a safe and effective treatment of shoulder pain associated with arthritic shoulder conditions, but its usefulness in a stroke population is unclear.
Methods—We undertook a randomized controlled trial assessing the effectiveness of SSNB in a population of 64 stroke patients (onset < 1 year) with hemiplegic shoulder pain. The primary outcome was pain measured on a visual analogue scale (VAS). Secondary outcomes were disability (Modified Rankin Scale, Croft Disability Index) and quality of life (EuroQol Health Questionnaire). All participants were assessed before randomization, and at 1, 4, and 12 weeks postintervention. Both groups continued with routine therapy.
Results—Although both intervention and control groups demonstrated reduction in pain score, participants who received SSNB consistently demonstrated superior, statistically significant pain reduction compared with placebo. Mean VAS reduction in the SSNB group was >18 mm greater than participants receiving placebo injection. The number needed to treat with SSNB to reduce 1 stroke survivor’s pain by 50% at 4 weeks is 4. No significant differences in function or quality of life were observed. No adverse events were reported.
Conclusions—Suprascapular nerve block is a safe and effective treatment for patients with hemiplegic shoulder pain.
Clinical Trial Registration—URL: Unique identifier: ACTRN12609000621213.