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, January 28, 2015

Beer compound could help fend off Alzheimer’s

But will your doctor tell you about this and wines' benefits?
The health-promoting perks of wine have attracted the spotlight recently, leaving beer in the shadows. But scientists are discovering new ways in which the latter could be a more healthful beverage than once thought. They’re now reporting in the Journal of Agricultural and Food Chemistry that a compound from hops could protect brain cells from damage—and potentially slow the development of disorders such as Alzheimer’s and Parkinson’s diseases.
Jianguo Fang and colleagues note that mounting evidence suggests that oxidative damage to neuronal cells contributes to the development of diseases that originate in the brain. If scientists could find a way to guard these cells from this type of damage, they might be able to help prevent or slow down Alzheimer’s disease, Parkinson’s disease and other neurodegenerative conditions. One compound found in hops, called xanthohumol, has gotten the attention of researchers for its potential benefits, including antioxidation, cardiovascular protection and anticancer properties. Fang’s team decided to test xanthohumol’s effects on brain cells.
In lab tests, the researchers found that the compound could protect neuronal cells and potentially help slow the development of brain disorders. The scientists conclude xanthohumol could be a good candidate for fighting such conditions.
Source: American Chemical Society

Nanoparticle that Lights Up Artery-Clogging Plaque to be Evaluated

This would be great and might have been able to find mine prior. The highlighted comment on inflammation is wrong. Inflammation causes the problems with atherscelerosis. I wish people would learn about cause and effect.
You can see a video of how plaque forms here:
Inflammation In Atherosclerotic Plaque Formation 
The Food and Drug Administration (FDA) has approved for evaluating in people a nanoparticle-based imaging agent jointly developed at Washington University School of Medicine in St. Louis and the University of California, Santa Barbara, in collaboration with Texas A&M University. The imaging agent may illuminate dangerous plaque in arteries, and doctors hope to use it to identify patients at high risk of stroke.
“This is the first receptor-targeted nanoparticle agent for cardiovascular imaging approved for investigational use in humans,” said principal investigator Pamela K. Woodard, MD, professor of radiology and of biomedical engineering. “Starting with bench research, then developing and testing the agent and taking it through the FDA process into human patients has involved an extensive team of basic scientists, clinical researchers and clinicians.”
In patients with atherosclerosis, plaque accumulates on the inner walls of arteries that deliver blood to the body.
“Plaque is a complex structure, made up of cholesterol, calcified deposits and other substances, all of which can cause inflammation,” said Woodard, also director of the Center for Clinical Imaging Research at the Mallinckrodt Institute of Radiology at Washington University. “Depending on the severity of the inflammation, these plaques can be stable or progress to a vulnerable phase in which they rupture, leading to stroke or heart attack.”
According to Woodard, many studies have indicated that most patients with plaque narrowing a carotid artery won’t go on to have a stroke.
“With current technology — such as ultrasound — we can’t tell whether the plaque is vulnerable or stable,” she said. “So we can’t distinguish the high-risk patients who need surgery from low-risk patients who can be treated with medication alone. We designed this nanoparticle agent to develop a test that can detect these vulnerable plaques and identify those patients at highest risk of stroke and in need of surgery to remove the plaque.”
This nanoparticle agent illuminates plaque in any of the body’s arteries and can be detected with a standard imaging technique called a positron emission tomography (PET) scan. Researchers recently began testing the safety of the nanoparticle in healthy individuals. They next will focus on patients with atherosclerosis who already are scheduled to undergo surgery to remove plaque from their carotid arteries.
“In this way, we’ll be able to see whether the areas that light up in the image because of our nanoparticles are the same areas that contain vulnerable plaque, as assessed from the surgeries,” Woodard said. “Once we show success imaging the carotid arteries, we will evaluate the nanoparticle agent in other vessels such as the coronary arteries, which represent a greater challenge because of their smaller size and complex motion.”
The nanoparticle is unique in how it is targeted, according to Yongjian Liu, PhD, assistant professor of radiology and co-investigator on the project. Previous research demonstrated that a receptor called NPR-C is present on the surface of cells that line blood vessels and is increased in atherosclerotic plaque. So the investigators added a small molecule to the nanoparticle that seeks out and binds to NPR-C, specifically targeting the particle to potentially dangerous plaque.
The nanoparticle also carries copper atoms, making it visible with a standard PET scanner. Similar small amounts of copper-64 regularly are used in PET scans, a technique common in cancer detection and therapy and neurologic imaging.
In addition, components of the nanoparticle also are designed to self-assemble in the watery environment of blood.
“The success of this nanoparticle system relies on the controlled self-assembly of functional polymers in water, which is driven by the careful design of hydrophilic (water-attracting) and hydrophobic (water-repelling) segments into the polymers,” said Craig J. Hawker, PhD, professor and director of the California Nanosystems Institute at the University of California, Santa Barbara. 
Added Woodard: “We have been able to develop this highly receptor-specific imaging technology because of the generous support from the National Heart, Lung and Blood Institute, our diverse and dedicated team of investigators and our extensive facilities that allow us to make this nanoparticle imaging agent in a sterile environment, meeting the FDA requirements for use in people.” 
According to the university’s Office of Technology Management, Pamela K. Woodard, Geoffrey E. Woodard, Rafaella Rossin and the late Michael J. Welch are the inventors of the patented NPR-C imaging method.


Cardiac Rehabilitation Phases

Where are the Stroke ones? That's right we have no stroke protocols at all because of the f*ckingly stupid belief in; 'All strokes are different, all stroke recoveries are different'.
1. Inpatient (acute) phase
2. Outpatient (sub-acute) phase3 to 6 months
3. Maintenance program and home phase

The 18 Habits of Highly Creative People

If we are going to solve the stroke medical problem WE are going to have to be incredibly creative. Does your doctor fall into these categories at all? Is your doctor a visionary or a caretaker?
While there’s no “typical” creative type, there are some tell-tale characteristics and behaviors of highly creative people. Here are 18 things they do differently.

1.  They daydream.

2. They observe everything.

3.  They work the hours that work for them.

4.  They take time for solitude.

5.  They turn life’s obstacles around.

6.  They seek out new experiences.

7.  They “fail up.”

8.  They ask the big questions.

9.  They people-watch.

10.  They take risks.

11.  They view all of life as an opportunity for self-expression.

12.  They follow their true passions.

13.  They get out of their own heads.

14.  They lose track of the time.

15.  They surround themselves with beauty.

16.  They connect the dots.

17.  They constantly shake things up.

18.  They make time for mindfulness.

Fully fleshed out at the link.


28 Arkansas Hospitals Recognized for Stroke Care Performance

What a bunch of f*cking lies. This is not recognizing results, this is recognizing doing processes which is a bunch of  crap.  Everyone involved here would be fired under my watch.
You only focus on guidelines when you can't promote your results. If they were any good at all they would tell you their 30 day death rates, tPA efficacy percentage and full recovery percentage. But YOU are going to have to call the hospital presidents and tell them that this is totally unacceptable. If you don't light a fire under our stroke hospitals your next stroke recovery will be as bad as your current one.
Guidelines here: You can see how this is nothing to be impressed about. This is all indirect action, not results.
Big f*cking whoopee.
The Arkansas Department of Health has recognized 28 hospitals (see list attached above or click here to read) with awards for stroke care performance as documented in the Arkansas Stroke Registry (ASR) between July 2013 and June 2014. The awards were given to hospitals meeting 90 percent or more of the stroke care performance measures(not RESULTS), with at least six stroke patients treated between July 2013 and June 2014.

The performance measures are American Heart Association/American Stroke Association-endorsed quality and achievement measures of the Get with the Guidelines-Stroke Patient Management Tool. The measures are benchmarked according to the standards of evidence-based stroke care guidelines to assure stroke patients receive appropriate and timely care.   (not RESULTS)

Tuesday, January 27, 2015

Your brain is hardening your arteries, but not on purpose!

Interesting writeup. Your doctor should be able to tell you how to handle this information. Demand a stroke protocol.
The team of researchers looked at how the infusion of oleic acid, a naturally occurring monounsaturated fatty acid, in the brain “triggers” a signal from the hypothalamus to the liver to lower its fat secretion, which researchers say is a “triglyceride-rich, very-low-density lipoprotein.

More at link.

Cumulative Use of Strong Anticholinergics and Incident Dementia

You probably have to consult with your doctor to make sure you aren't increasing your dementia risk.
Abstract here:
Cumulative Use of Strong Anticholinergics and Incident Dementia

Readable PSYblog here:

4 Very Common Medicines Newly Linked to Irreversible Dementia Risk

Four commonly used drugs which have strong anticholinergic effects are:
  1. Doxepin (Sinequan) – an older antidepressant.
  2. Chlorpheniramine (Chlor-Trimeton) – an antihistamine used to treat hayfever.
  3. Diphenhydramine (Benadryl) – another antihistamine often used to treat hayfever and sometimes used to aid sleep.
  4. Oxybutynin (Ditropan) – for bladder control.
The study, which is published in JAMA Internal Medicine, tracked 3,434 people over the age of 65 who had no signs of dementia (Gray et al., 2015).
They were followed up over 7 years, during which time 797 developed dementia.


Monday, January 26, 2015

Trivia rehabilitation

Once again I wonder how much I should push my answers.
One of the questions tonight;
Whi ch country had the first female prime minister?
A. Britain
B. Australia
C. India
D. Sri Lanka

I choose C and explained my reasoning behind it. The other 7 persons there agreed and we put in the answer. One person suggested D.
The answer is D. The person who suggested D. said, 'That's right, Dean is better at arguing he's right than being right'.   I once convinced a friend three times in a row to use my answer rather than his hunches. He has resolved never to play trivia with me again.
We were still successful tonight 2nd out of 17 teams.

Deficiency of Brain ATP-Binding Cassette Transporter A-1 Exacerbates Blood–Brain Barrier and White Matter Damage After Stroke

Is your doctor testing for this post-stroke to remedy this deficiency so your next stroke won't be so bad? Does your doctor have any clue that this problem even exists?

  1. Jieli Chen, MD
+ Author Affiliations
  1. From the Department of Neurology, Henry Ford Hospital, Detroit, MI (X.C., M.C., A.Z., Y.C., R.N., Y.Z., J.C.); Department of Physics, Oakland University, Rochester, MI (M.C.); Neural Protection and Regeneration section, Center for Neuropsychiatric Research, National Institute on Drug Abuse, NIH, Baltimore, MD (Y.W.); and Department of Medical Genetics, Centre for Molecular Medicine and Therapeutics, University of British Columbia, Vancouver, British Columbia, Canada (J.M.K.).
  1. Correspondence to Xu Cui, MD, PhD, Neurology Research, E&R Bldg, Room No. 3029, Henry Ford Hospital, 2799 West Grand Blvd, Detroit, MI 48202, E-mail or Jieli Chen, MD, Department of Neurology, Henry Ford Hospital, Detroit, MI 48202, E-mail


Background and Purpose—The ATP-binding cassette transporter A-1 (ABCA1) gene is a key target of the transcription factors liver X receptors. Liver X receptor activation has anti-inflammatory and neuroprotective effects in animal ischemic stroke models. Here, we tested the hypothesis that brain ABCA1 reduces blood–brain barrier (BBB) and white matter (WM) impairment in the ischemic brain after stroke.
Methods—Adult brain-specific ABCA1–deficient (ABCA1−B/−B) and floxed-control (ABCA1fl/fl) mice were subjected to permanent distal middle cerebral artery occlusion and were euthanized 7 days after distal middle cerebral artery occlusion. Functional outcome, infarct volume, BBB leakage, and WM damage were analyzed.
Results—Compared with ABCA1fl/fl mice, ABCA1−B/−B mice showed marginally (P=0.052) increased lesion volume but significantly increased BBB leakage and WM damage in the ischemic brain and more severe neurological deficits. Brain ABCA1–deficient mice exhibited increased the level of matrix metalloproteinase-9 and reduced the level of insulin-like growth factor 1 in the ischemic brain. BBB leakage was inversely correlated (r=−0.073; P<0.05) with aquaporin-4 expression. Reduction of insulin-like growth factor 1 and aquaporin-4, but upregulation of matrix metalloproteinase-9 expression were also found in the primary astrocyte cultures derived from ABCA1−B/−B mice. Cultured primary cortical neurons derived from C57BL/6 wild-type mice with ABCA1−B/−B astrocyte–conditioned medium exhibited decreased neurite outgrowth compared with culture with ABCA1fl/fl astrocyte–conditioned medium. ABCA1−B/−B primary cortical neurons show significantly decreased neurite outgrowth, which was attenuated by insulin-like growth factor 1 treatment.
Conclusions—We demonstrate that brain ABCA1 deficiency increases BBB leakage, WM/axonal damage, and functional deficits after stroke. Concomitant reduction of insulin-like growth factor 1 and upregulation of matrix metalloproteinase-9 may contribute to brain ABCA1 deficiency–induced BBB and WM/axonal damage in the ischemic brain.

National Institutes of Health Stroke Scale Item Profiles as Predictor of Patient Outcome

I can't see how using this scale has any use whatsoever. There is nothing objective about it. If we are ever going to be able to compare strokes we are going to have to have scans of the brain showing dead and damaged areas. That would finally allow us to match stroke protocols to what actually worked for recovery. And we could get away from the appallingly stupid meme of 'All strokes are different, all stroke recoveries are different'.

External Validation on Independent Trial Data

  1. Kennedy R. Lees, MD;
  2. for the VISTA Collaborators
+ Author Affiliations
  1. From the Institute of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow, United Kingdom (A.H.A.-R., R.L.F., K.R.L.); Division of Biostatistics and Epidemiology, Cincinnati Children’s Hospital Medical Centre, OH (H.S.); Department of Neurology, University of Cincinnati College of Medicine, OH (D.K., P.K., J.P.B.).
  1. Correspondence to Azmil H. Abdul-Rahim, MRCP, MBChB, Institute of Cardiovascular and Medical Sciences, University of Glasgow, 44 Church St, G11 6NT Glasgow, United Kingdom. E-mail


Background and Purpose—National Institutes of Health Stroke Scale (NIHSS) item profiles that were recently proposed may prove useful both clinically and for research studies. We aimed to validate the NIHSS item profiles in an acute cohort.
Methods—We conducted a retrospective analysis on pooled data from randomized clinical trials. We applied the latent class analysis probabilities of profile membership developed from the derivation study to obtain symptom grouping, a-NIHSS item profiles. We implemented an independent latent class analysis to derive secondary symptom grouping, b-NIHSS item profiles. Validation was performed by assessing the associations with outcomes and evaluating both sets of NIHSS item profiles’ discrimination and calibration to the data. The outcomes evaluated included modified Rankin Scale (mRS; using the full distribution and dichotomized, mRS, 0–1) at day 90 and mortality by 90 days.
Results—We identified 10 271 patients. Ordinal analysis of mRS confirmed increased odds of better outcome across the profiles in a stepwise manner, adjusted for age and thrombolysis treatment, for each set of NIHSS item profiles. Similar patterns were observed for mRS 0 to 1, and inverse patterns were seen for mortality. The c-statistics of a-NIHSS and b-NIHSS item profiles for mRS 0 to 1 were similar at 0.71 (95% confidence interval, 0.70–0.72) and for mortality, 0.74 (0.73–0.75) and 0.75 (0.73–0.76), respectively. Calibration was good.
Conclusions—These NIHSS item profiles identified using latent class analysis offer a reliable approach to capture the true response patterns that are associated with functional and outcome and mortality post stroke. This approach has the potential to enhance the clinical value of the overall NIHSS score.

Novel insights into the rehabilitation of memory post acquired brain injury: a systematic review

So which of these training approaches is in your doctors stroke protocol for memory?
Lauriane A. Spreij1, Johanna M. A. Visser-Meily2, Caroline M. van Heugten3 and Tanja C. W. Nijboer1,2*
  • 1Department of Experimental Psychology, Helmholtz Institute, Utrecht University, Utrecht, Netherlands
  • 2Brain Center Rudolf Magnus, Center of Excellence for Rehabilitation Medicine, University Medical Center Utrecht, and De Hoogstraat Rehabilitation, Utrecht, Netherlands
  • 3Department of Psychiatry and Neuropsychology, Faculty of Health, Medicine and Life Sciences, Maastricht University, Maastricht, Netherlands
Objective: Acquired Brain Injury (ABI) frequently results in memory impairment causing significant disabilities in daily life and is therefore a critical target for cognitive rehabilitation. Current understanding of brain plasticity has led to novel insights in remediation-oriented approaches for the rehabilitation of memory deficits. We will describe 3 of these approaches that have emerged in the last decade: Virtual Reality (VR) training, Computer-Based Cognitive Retraining (CBCR) and Non-Invasive Brain Stimulation (NBS) and evaluate its effectiveness.
Methods: A systematic literature search was completed in regard to studies evaluating interventions aiming to improve the memory function after ABI. Information concerning study content and reported effectiveness were extracted. Quality of the studies and methods were evaluated.
Results: A total of 786 studies were identified, 15 studies met the inclusion criteria. Three of those studies represent the VR technique, 7 studies represent CBCR and 5 studies NBS. All 3 studies found a significant improvement of the memory function after VR-based training, however these studies are considered preliminary. All 7 studies have shown that CBCR can be effective in improving memory function in patients suffering from ABI. Four studies of the 5 did not find significant improvement of the memory function after the use of NBS in ABI patients.
Conclusion: On the basis of this review, CBCR is considered the most promising novel approach of the last decade because of the positive results in improving memory function post ABI. The number of studies representing VR were limited and the methodological quality low, therefore the results should be considered preliminary. The studies representing NBS did not detect evidence for the use of NBS in improving memory function.

Development and evaluation of a self-administered on-line test of memory and attention for middle-aged and older adults

Your doctor should be extremely familiar with these in order to get you into the right stroke protocol to prevent your descent into dementia.
Angela K. Troyer1,2*, Gillian Rowe1,2, Kelly J. Murphy1,2, Brian Levine2,3, Larry Leach1 and Lynn Hasher2,3
  • 1Neuropsychology and Cognitive Health Program, Baycrest Centre for Geriatric Care, Toronto, ON, Canada
  • 2Department of Psychology, University of Toronto, Toronto, ON, Canada
  • 3Rotman Research Institute, Baycrest Centre for Geriatric Care, Toronto, ON, Canada
There is a need for rapid and reliable Internet-based screening tools for cognitive assessment in middle-aged and older adults. We report the psychometric properties of an on-line tool designed to screen for cognitive deficits that require further investigation. The tool is composed of measures of memory and executive attention processes known to be sensitive to brain changes associated with aging and with cognitive disorders that become more prevalent with age. Measures included a Spatial Working Memory task, Stroop Interference task, Face-Name Association task, and Number-Letter Alternation task. Normative data were collected from 361 healthy adults age 50–79 who scored in the normal range on a standardized measure of general cognitive ability. Participants took the 20-minute on-line test on their home computers, and a subset of 288 participants repeated the test 1 week later. Analyses of the individual tasks indicated adequate internal consistency, construct validity, test-retest reliability, and alternate version reliability. As expected, scores were correlated with age. The four tasks loaded on the same principle component. Demographically-corrected z-scores from the individual tasks were combined to create an overall score, which showed good reliability and classification consistency. These results indicate the tool may be useful for identifying middle-aged and older adults with lower than expected scores who may benefit from clinical evaluation of their cognition by a health care professional.

More at link including references.

U.S. government unveils goal to move Medicare away from fee-for-service

If the US would follow this for stroke rehab there would probably pay for only the 10% full recovery rate. Our doctors would state that their work is what caused the normal spontaneous recovery and fraudulently claim payments for that. Right now if pay for performance would exist there would not be a neurologist paid for anything in stroke rehab. I bet this will still not be enough for our stroke medical system to come up with effective stroke protocols. Stroke survivors are totally f*cking screwed until the complete stroke medical world is replaced.

A Forbes article on the same thing.

Medicare's Bolt From Fee-For-Service Medicine, Means 50 Percent Value Pay By 2018

Interleukin-6 and C-reactive protein as predictors of cognitive decline in late midlife

Can your doctor use this to address your 33% dementia chance post-stroke from an Australian study?



Peripheral inflammatory markers are elevated in patients with dementia. In order to assess their etiologic role, we examined whether interleukin-6 (IL-6) and C-reactive protein (CRP) measured in midlife predict concurrently assessed cognition and subsequent cognitive decline.


Mean value of IL-6 and CRP, assessed on 5,217 persons (27.9% women) in 1991-1993 and 1997-1999 in the Whitehall II longitudinal cohort study, were categorized into tertiles to examine 10-year decline (assessments in 1997-1999, 2002-2004, and 2007-2009) in standardized scores (mean = 0, SD = 1) of memory, reasoning, and verbal fluency using mixed models. Mini-Mental State Examination (MMSE) was administered in 2002-2004 and 2007-2009; decline ≥3 points was modeled with logistic regression. Analyses were adjusted for baseline age, sex, education, and ethnicity; further analyses were also adjusted for smoking, obesity, Framingham cardiovascular risk score, and chronic diseases (cancer, coronary heart disease, stroke, diabetes, and depression).


In cross-sectional analysis, reasoning was 0.08 SD (95% confidence interval [CI] -0.14, -0.03) lower in participants with high compared to low IL-6. In longitudinal analysis, 10-year decline in reasoning was greater (ptrend = 0.01) among participants with high IL-6 (-0.35; 95% CI -0.37, -0.33) than those with low IL-6 (-0.29; 95% CI -0.31, -0.27). In addition, participants with high IL-6 had 1.81 times greater odds ratio of decline in MMSE (95% CI 1.20, 2.71). CRP was not associated with decline in any test.


Elevated IL-6 but not CRP in midlife predicts cognitive decline; the combined cross-sectional and longitudinal effects over the 10-year observation period corresponded to an age effect of 3.9 years.

The Preventive Antibiotics in Stroke Study (PASS): a pragmatic randomised open-label masked endpoint clinical trial

I couldn't figure out what these antibiotics were supposed to do to possibly  have better functional outcomes. So ask your doctor who should know.



In adults with acute stroke, infections occur commonly and are associated with an unfavourable functional outcome. In the Preventive Antibiotics in Stroke Study (PASS) we aimed to establish whether or not preventive antimicrobial therapy with a third-generation cephalosporin, ceftriaxone, improves functional outcome in patients with acute stroke.


In this multicentre, randomised, open-label trial with masked endpoint assessment, patients with acute stroke were randomly assigned to intravenous ceftriaxone at a dose of 2 g, given every 24 h intravenously for 4 days, in addition to stroke unit care, or standard stroke unit care without preventive antimicrobial therapy; assignments were made within 24 h after symptom onset. The primary endpoint was functional outcome at 3 months, defined according to the modified Rankin Scale and analysed by intention to treat. The primary analysis was by ordinal regression of the primary outcome. Secondary outcomes included death, infection rates, antimicrobial use, and length of hospital stay. Participants and caregivers were aware of treatment allocation but assessors of outcome were masked to group assignment. This trial is registered with, number ISRCTN66140176.


Between July 6, 2010, and March 23, 2014, a total of 2550 patients from 30 sites in the Netherlands, including academic and non-academic medical centres, were randomly assigned to the two treatment groups: 1275 patients to ceftriaxone and 1275 patients to standard treatment (control group). 12 patients (seven in the ceftriaxone group and five in the control group) withdrew consent immediately after randomisation, leaving 2538 patients available for the intention-to-treat-analysis (1268 in the ceftriaxone group and 1270 in the control group). 2514 (99%) of 2538 patients (1257 in each group) completed 3-month follow-up. Preventive ceftriaxone did not affect the distribution of functional outcome scores on the modified Rankin Scale at 3 months (adjusted common odds ratio 0·95 [95% CI 0·82–1·09], p=0·46). Preventive ceftriaxone did not result in an increased occurrence of adverse events. Overgrowth infection with Clostridium difficile occurred in two patients (<1%) in the ceftriaxone group and none in the control group.


Preventive ceftriaxone does not improve functional outcome at 3 months in adults with acute stroke. The results of our trial do not support the use of preventive antibiotics in adults with acute stroke.


Netherlands Organization for Health Research and Development, Netherlands Heart Foundation, and the European Research Council.

To read this article in full you will need to make a payment

Sunday, January 25, 2015

Brain Region Discovered That Stops You Being a Couch Potato

Has this region been damaged in your stroke or do you just have garden variety stroke fatigue? What stroke protocol does your doctor have for either condition? ANY AT ALL?
The area of the brain which may control the motivation to exercise — along with other rewarding activities — has been identified by a new study.
The tiny area of the brain, called the dorsal medial habenula, was found to control mice’s motivation to exercise (Turner et al., 2014).

More at link.

Colorado Doctor Discovered Natural Way To Treat Common Vertigo

Notice that it says common vertigo. Do not try this without your doctors ok

Multitasking stroke rehab

Went to a Paula Cole concert tonight, the 1 hour ride down there and back involved many many flexions and extensions of my left hand fingers. The concert itself  had me either vibrating my left leg up and down or dorsiflexing my left foot. At the same time I flattened my left hand on my right thigh and used my right hand to keep it flat and have the thumb extended away from the first finger.  Your doctor if any good at all would know how many hours you need to hold your spastic hand flat to stop the spasticity. But they know absolutely f*cking nothing about how to cure spasticity.
Stopped at the Jolly Pumkin afterwards and had a berserker.
Chris Bruce Ben Wittman Paula Cole

The beserker glass

Saturday, January 24, 2015

How Does Post-Traumatic Stress Disorder Change the Brain?

With your chance of  PTSD following stroke of 23%
this article assumes that PTSD only comes from near death experiences so you'll have to read it with that bias in mind. 

Cohen's Brain Bits: Waiting for Charcot Wearable technology may be a boon to patients with neurologic disorders.

You'll have to ask your doctor  if the Parkinson's shoe would be helpful for your walking needs.  Does your doctor even know about this or anything new at all? Has your doctor changed or created any stroke protocols in the last 10 years? If not, they should be fired.
If we don't start firing doctors for not keeping up with new research they will never change. Call the hospital president when you find such incompetent doctors. Yes I know this is not a way to ingratiate myself with the stroke medical world, but I don't want to interact with doctors that don't keep up-to-date.

Friday, January 23, 2015

Anthony Jay once said something like "You can judge a leader by the size of the problems they tackle."

From a Gapingvoid art piece;
Our stroke associations don't seem to be tackling any problems whatsoever. In fact, my opinion is that they are hiding from stroke survivors. They are afraid to talk to us. CHICKENSHITS!!!
This telling the truth is no way to get them to actually work with us though. I'm looking at you; ASA, NSA, WSO.

UnitedHealth's $43 Billion Exit From Fee-For-Service Medicine

If United Health would follow this for stroke rehab there would probably pay for only the 10% full recovery rate. Our doctors would state that their work is what caused the normal spontaneous recovery and fraudulently claim payments for that. Right now if pay for performance would exist there would not be a neurologist paid for anything in stroke rehab. I bet this will still not be enough for our stroke medical system to come up with effective stroke protocols. Stroke survivors are totally f*cking screwed until the complete stroke medical world is replaced.

Viewing photos and reading nouns of natural graspable objects similarly modulate motor responses

Would this be the first stroke protocol to try for those movements you can't do. Then action observation and passive movement. What exact stroke protocols is your doctor having you follow to recover movements you don't have due to dead brain?
Do not do anything like this on your own, you know how dangerous viewing pictures are without your doctors guidance.
Barbara F. M. Marino1,2, Miriam Sirianni3,4, Riccardo Dalla Volta4, Fabio Magliocco4, Francesco Silipo4, Aldo Quattrone4 and Giovanni Buccino3,4*
  • 1Dipartimento di Neuroscienze, Sezione di Fisiologia, Università di Parma, Parma, Italy
  • 2Dipartimento di Psicologia, University Milano Bicocca, Milano, Italy
  • 3IRCCS Neuromed, Pozzilli, Italy
  • 4Dipartimento di Scienze Mediche e Chirurgiche, Università “Magna Graecia” di Catanzaro, Germaneto, Italy
It is well known that the observation of graspable objects recruits the same motor representations involved in their actual manipulation. Recent evidence suggests that the presentation of nouns referring to graspable objects may exert similar effects. So far, however, it is not clear to what extent the modulation of the motor system during object observation overlaps with that related to noun processing. To address this issue, 2 behavioral experiments were carried out using a go-no go paradigm. Healthy participants were presented with photos and nouns of graspable and non-graspable natural objects. Also scrambled images and pseudowords obtained from the original stimuli were used. At a go-signal onset (150 ms after stimulus presentation) participants had to press a key when the stimulus referred to a real object, using their right (Experiment 1) or left (Experiment 2) hand, and refrain from responding when a scrambled image or a pseudoword was presented. Slower responses were found for both photos and nouns of graspable objects as compared to non-graspable objects, independent of the responding hand. These findings suggest that processing seen graspable objects and written nouns referring to graspable objects similarly modulates the motor system.


It is known that hand-object interactions recruit a parieto-frontal circuit in the brain of both monkeys and humans subserving sensorimotor transformations (Rizzolatti et al., 1981, 1988, 2002; Kurata and Tanji, 1986; Taira et al., 1990; Hepp-Reymond et al., 1994; Jeannerod et al., 1995; Sakata et al., 1995; Binkofski et al., 1999; Grol et al., 2007; Hecht et al., 2013). Also the mere observation of objects that have the potential for being manipulated has been proven to be effective in modulating the activity of the motor system. Single-unit recording studies in monkeys have shown that a set of neurons known as “canonical neurons” discharges during the presentation of graspable objects (Rizzolatti et al., 1988; Murata et al., 1997; Raos et al., 2006; Umiltà et al., 2007). In keeping with this, brain imaging studies have shown the activation of fronto-parietal areas in the human brain during the observation of graspable objects (Chao and Martin, 2000; Grèzes et al., 2003a,b). The recruitment of the motor system during object observation is fine-tuned with the intrinsic features of objects that make them appropriate for manual action: for example motor evoked potentials (MEPs) recorded during the observation of graspable objects (e.g., a mug) with a broken handle were significantly different from MEPs recorded during the observation of a complete object (Buccino et al., 2009).

Much more at link.

Revolutionary device found to lower blood pressure

I may have to send this to my dad.
But what about this?
The One Benefit Of High Blood Pressure? It May Prevent Dementia

Revolutionary device found to lower blood pressure
A revolutionary device has been shown to significantly lower blood pressure among patients with uncontrolled high blood pressure, compared to those treated with usual drug measures – according to research from Queen Mary University of London and published in The Lancet.
The device – developed by ROX Medical and named the ‘Coupler’ – is a paper clip sized implant which is inserted between the artery and vein in the upper thigh, in a procedure lasting around 40 minutes under local anaesthetic.
Researchers led a randomised, blinded endpoint clinical trial with patients from multiple European Centres of Hypertension Excellence – including the Barts Blood Pressure Clinic at Barts Health NHS Trust in east London – all of whom had resistant high blood pressure and had not responded to at least three types of drug treatment.
The team compared the effects of the Coupler versus usual medical treatment in 83 patients of whom 44 received the ROX Coupler therapy. Patients who received the Coupler experienced a significant and durable reduction in blood pressure. There was also a reduced number of hypertensive complications and hospital admissions for high blood pressure crises.

More at link.

Samsung prototypes brainwave-reading wearable stroke detector

I wonder if this can be calibrated for those of us that already have brain damage so it could measure new brain damage?
Would this new one be any better than these 17 ways for objective diagnosis.
A group of Samsung engineers have come up with a plan to harness the power of your phone or tablet to warn you of an impending stroke. By monitoring your brainwaves the system would detect the early signs of a stroke, and could one day be built into your glasses to keep you safe all the time.
A stroke happens when the blood supply to part of your brain is cut off by a clot or damaged by a bleed, which causes brain cells in the affected area to die. According to the World Health Organisation, 15 million people across the world suffer from a stroke each year. Around 66 per cent of those people die or are left with permanent physical disabilities.
To combat the problem, five Samsung engineers have come up with a prototype system called Early Detection Sensor & Algorithm Package (EDSAP). There are two parts to the system: a headset, covered in sensors that record electrical impulses in the brain; and a mobile app, in which an algorithm analyses the brainwaves and, in less than a minute, determines the likelihood of a stroke.
The project started two years ago when a group of Samsung smartphone and washing machine engineers fancied a change and banded together to look at the problem of stroke. Despite doctors being "dismissive", the engineers decided to take the project to Samsung's Creativity Lab, or C-Lab. C-Lab helps Samsung employees turn creative or quirky ideas into potentially commercial products.
The Samsung team reckon they've improved on current medical methods with the headset, which is made from a conductive and comfortable rubber-like material that doesn't require a saline solution rubbed onto your head.
In theory, the rubber material is versatile enough to make other things instead of a headset -- for example, sensors could be put into hairpins or eyeglasses so you can wear them all the time and monitor your brainwaves constantly.
As well as providing an early warning about the possibility of a stroke, the system can analyse stress and sleep patterns. The principles of EDSAP could also potentially be used to monitor electrocardiograms -- heartbeats -- so the team is looking at how the technology could be used to monitor your heart.
However, EDSAP is still at the very earliest stages, with clinical trials among the steps to be taken before EDSAP technology is ready for the public.
"Stroke is not inevitable," says Joe Korner, Director of External Affairs at the Stroke Association. "In many cases there are simple steps people can take to reduce their risk of stroke such as keeping their blood pressure under control, eating a balanced diet and exercising more. Anyone with any concerns about their risk of stroke should have a chat with their GP."
When someone has a stroke it's vital they receive emergency medical treatment as soon as possible. "If you think someone is having a stroke," advises Korner, "you can use the FAST test to recognise the signs:

AHA Skeptical on Salt Study

I'm sure your doctor won't be changing your blood pressure protocols just yet but ask about this newest one or these other articles. But never mind, YOU are not to research medical stuff on your own, your doctor is the gatekeeper and you must obey.
You can have your doctor compare this new headline to these:

The wrong white crystals: not salt but sugar as aetiological in hypertension and cardiometabolic disease

Salt May Not Be a Demon After All

 AHA Skeptical on Salt Study

Thursday, January 22, 2015

The New Years resolution is going to be blown soon

I've been trying to keep a running total of 70,000 steps per week, thru today I've succeeded. I'm going to have to let it lapse. My foot pain is getting to the point that standing up after sitting for a while causes the leg to collapse. If I get walking I can keep going because the pain is regular. I'm hoping whatever it is will resolve in a week or two, then I'll take the walking up again.

Patients Creating Meaningful Solutions for their Own Disease

This is the only f*cking way stroke will be solved. The existing stroke associations are worse than useless. This quote from Amy Farber is instructive.
For the past five years Farber has been battling not only her own disease(LAM, lymph-angiolio-myomatosis.) but also the wall of resistance erected by those who believe that a patient can make about as much of a meaningful contribution to the process of scientific discovery as a laboratory rat.

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

If this truly works how many years before your hospital creates a stroke protocol on this. Do not do this on your own. You know how dangerous foot baths would be if it is not prescribed by your doctor.
I'm betting 50 years. I would ask for testing of this on hand and arms. But I have no place to ask for such testing because we have crap for stroke associations.
1) Department of Rehabilitation and Physical Medicine, Graduate School of Medical and Dental Sciences, Kagoshima University
Released 20150115  
  • Abstracts

Objectives: Spasticity is defined as a pathological increase in muscle tonus, and increased muscle tonus of lower limbs is a major obstacle to the stroke rehabilitation. Foot baths are considered to provide beneficial thermal therapy for post-stroke patients with spasticity, but their anti-spastic effects have not been investigated comprehensively. The present study aimed to evaluate alterations in spasticity and motor function using foot baths in post-stroke patients with spastic hemiplegia.
Methods: We underwent two separate experiments each consisting of immersion in warm water up to the knee joint level, and measuring spasticity, physiological examination and motor function.
Experiment 1; Fourteen post-stroke patients with lower limb spasticity were enrolled in this study (nine males and five females; mean age 50.4±12.9 years; range, 28-65 years). The subjects’ legs from below the knee joint were immersed in water at 41°C for 15 min. Measurements of F-waves and a physiological examination were carried out immediately (within 5 min) after the foot-bath session, and again 30 min later, while the subject remained wrapped in blankets on the lift-bath stretcher.
Experiment 2; Six post-stroke patients with lower limb spasticity were enrolled in this study (five males and one female; mean age 55.2±14.6 years; range, 39-68 years). The subjects’ legs from below the knee joint were immersed in the artificial high concentration carbon-dioxide (CO2) water or tap water foot bath at 38°C for 30 min. Measurements of muscle stiffness, motor function (active range of motion: A-ROM) and a physiological examination were carried out immediately (within 5 min) after the foot-bath session, and again 10 min later, while the subject remained wrapped in blankets.
Results: None of the subjects experienced discomfort before, during or after the foot-bath treatment. The physiological examination was completed safely in all subjects.
Experiment 1; The mean values of F-wave parameters were significantly reduced after foot-bath treatment (P<0.01). The anti-spastic effects of foot-bath treatment were indicated by decreased F-wave parameters, in parallel with decreases in modified Ashworth scale (MAS) score. The body temperature was significantly increased both immediately after, and 30 min following foot-bath treatment.
Experiment 2; The changes both in the body and surface skin temperature were higher in the artificial high concentration CO2 water foot bath compared with the tap water foot bath. The changes in the MAS score, muscle stiffness and A-ROM were also higher in the high concentration CO2 water foot bath than in the tap water foot bath.
Conclusion: These findings demonstrate that the use of foot baths is an effective non-pharmacological anti-spastic treatment that might facilitate stroke rehabilitation. In addition, the high concentration CO2 water foot baths appeared to play an important role in decreased spasticity.

Puerarin protects brain tissue against cerebral ischemia/reperfusion injury by inhibiting the inflammatory response

This is going to be hard to implement in humans - 30 minutes before middle cerebral artery occlusion and 8 hours after reperfusion.;year=2014;volume=9;issue=23;spage=2074;epage=2080;aulast=Zhou
Correspondence Address:
Yuanyuan Yao
Department of Anesthesiology, Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou 310009
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DOI: 10.4103/1673-5374.147934
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Puerarin, a traditional Chinese medicine, exerts a powerful neuroprotective effect in cerebral ischemia/reperfusion injury, but its mechanism is unknown. Here, we established rat models of middle cerebral artery ischemia/reperfusion injury using the suture method. Puerarin (100 mg/kg) was administered intraperitoneally 30 minutes before middle cerebral artery occlusion and 8 hours after reperfusion. Twenty-four hours after reperfusion, we found that puerarin significantly improved neurological deficit, reduced infarct size and brain water content, and notably diminished the expression of Toll-like receptor-4, myeloid differentiation factor 88, nuclear factor kappa B and tumor necrosis factor-α in the ischemic region. These data indicate that puerarin exerts an anti-inflammatory protective effect on brain tissue with ischemia/reperfusion damage by downregulating the expression of multiple inflammatory factors.

Increased sleep need and daytime sleepiness 6 months after traumatic brain injury: a prospective controlled clinical trial

Whom can we go to to get this research duplicated for stroke? ASA? NSA? WSO? A huge percentage of survivors have fatigue and right now I don't think there is any protocol to address how to solve the fatigue problem. Telling you to get cardiovascularily fit does not solve the problem. I was considered as an athlete so my cardiovascular fitness was great even post-stroke. My fatigue was continuous.


Post-traumatic sleep-wake disturbances are common after acute traumatic brain injury. Increased sleep need per 24 h and excessive daytime sleepiness are among the most prevalent post-traumatic sleep disorders and impair quality of life of trauma patients. Nevertheless, the relation between traumatic brain injury and sleep outcome, but also the link between post-traumatic sleep problems and clinical measures in the acute phase after traumatic brain injury has so far not been addressed in a controlled and prospective approach. We therefore performed a prospective controlled clinical study to examine (i) sleep-wake outcome after traumatic brain injury; and (ii) to screen for clinical and laboratory predictors of poor sleep-wake outcome after acute traumatic brain injury. Forty-two of 60 included patients with first-ever traumatic brain injury were available for follow-up examinations. Six months after trauma, the average sleep need per 24 h as assessed by actigraphy was markedly increased in patients as compared to controls (8.3 ± 1.1 h versus 7.1 ± 0.8 h, P < 0.0001). Objective daytime sleepiness was found in 57% of trauma patients and 19% of healthy subjects, and the average sleep latency in patients was reduced to 8.7 ± 4.6 min (12.1 ± 4.7 min in controls, P = 0.0009). Patients, but not controls, markedly underestimated both excessive sleep need and excessive daytime sleepiness when assessed only by subjective means, emphasizing the unreliability of self-assessment of increased sleep propensity in traumatic brain injury patients. At polysomnography, slow wave sleep after traumatic brain injury was more consolidated. The most important risk factor for developing increased sleep need after traumatic brain injury was the presence of an intracranial haemorrhage. In conclusion, we provide controlled and objective evidence for a direct relation between sleep-wake disturbances and traumatic brain injury, and for clinically significant underestimation of post-traumatic sleep-wake disturbances by trauma patients.

More at link.

Doctor's Shocking Video Reveals: These 7 Things Trigger Alzheimer's in Your Brain

You can watch this video and the other ones to see if there is any reason at all to trust this guy.

Doctor's Shocking Video Reveals: These 7 Things Trigger Alzheimer's in Your Brain

This has lots of sales pitches for his Wellness Report. NO references to research at all. Flu vaccines should not be taken because of the toxic metals in them. Wow, what a load of ---. Even talked about detoxing your brain.

After 15 minutes I gave up because the sales pitch was overbearing, never did learn anything useful.

My complete list here:
Dementia prevention 19 ways

Other information to consider when deciding whether to trust anything he has to say;

Interview: Dr. Russell Blaylock Exposes Obama's Nazi Healthcare System

Quack of the Day: Dr. Russell Blaylock

Skeptics Dictionary - Russell Blaylock, M.D.



Wednesday, January 21, 2015

Blueberries, Avocados and Cocoa Beans May Keep Cardiologists at Bay

For your edification. You can start betting on how long it takes your hospital to add these as smoothies to your hospital diet. I'm betting 50 years. Don't do this on your own, you know how dangerous eating food is without your doctors prescription.

Sarah Bergbreiter: Why I make robots the size of a grain of rice

Hell you could send them on a cleanup mission to scrape the plaque off arterial walls. As long as you would be able to put them in reverse and they carry their garbage collected back out with them. Or maybe have them plug those bleeds. The possibilities are endless if we had any innovative thinkers at all within the stroke world.
By studying the movement and bodies of insects such as ants, Sarah Bergbreiter and her team build incredibly robust, super teeny, mechanical versions of creepy crawlies … and then they add rockets. See their jaw-dropping developments in micro-robotics, and hear about three ways we might use these little helpers in the future.

Is your cholesterol really too high?

A discussion topic with your doctor. Do not stop statins on your own.

Sound Mind, Strong Heart: Same Protein Sustains Both

So what protocol is your doctor giving you to make sure your BDNF levels are adequate? Does your doctor know anything about this? This is still only in rodents so 50 years before it makes it to humans unless YOU raise some hell to get it researched.
A Roman philosopher was the first to note the relationship between a sound mind and a sound body. Now the findings of a new Johns Hopkins study reveal a possible biochemical explanation behind this ancient observation.
The research, published ahead of print Jan. 12 in the Proceedings of the National Academy of Sciences, reveals that a protein already known to act as a natural antidepressant, enhance learning and memory, power nerve cell growth, and nourish blood vessels is also a central player in maintaining heart muscle vitality.
The team’s experiments, conducted in mice and lab-grown heart cells, show this multi-tasking protein, a nerve-growth factor called BDNF (brain-derived neurotrophic factor), helps sustain the ability of heart muscle cells to contract and relax properly. The results reveal that either BDNF deficiency or cell insensitivity to BDNF’s presence can precipitate heart muscle dysfunction, particularly under conditions of chronic or repeated physical stress on the heart, such as endurance training or high blood pressure. Specifically, the researchers tracked BDNF’s role in a cascade of molecular signaling events in heart cells, the disruption of which led to heart muscle failure.
If confirmed in humans, the research team says, the findings could pave the way to new treatments for certain forms of heart failure, a disorder that affects nearly 6 million Americans and more than 23 million people worldwide.
In addition, because of BDNF’s well-known antidepressant effects and its role as a booster of nerve cell health, the research teams says the results suggest a possible biochemical link between depression and heart disease, two disorders that tend to occur in concert but whose relationship remains poorly understood.
“Our results are not only a vivid reminder of the astounding complexity of the heart’s chemistry and physiology, but also a striking example of the ability of a single protein to act on multiple fronts and affect many organs and functions,” says lead investigator Ning Feng, M.D., Ph.D., a cardiology fellow at the Johns Hopkins University School of Medicine.
The findings also can help clarify the biological means behind recent – and unexplained –observations that heart failure patients whose cardiac function worsens during physical exertion have low levels of BDNF in the blood.
“Our observation that BDNF directly controls the ability of heart muscle cells to ‘beat’ properly offers one possible explanation behind the declining cardiac function seen in people with heart failure, especially during exercise,” says senior author Nazareno Paolocci, M.D., Ph.D., assistant professor of medicine at the Johns Hopkins University School of Medicine.
In an initial set of experiments, the scientists isolated cardiac cells from rodents with either normal or failing hearts in a lab dish and exposed the cells to BDNF. The normal heart cells responded by contracting and relaxing vigorously in the presence of BDNF, a phenomenon marked by peaks of contraction-triggering calcium flow into the cells. However, cells obtained from failing hearts, even when awash in BDNF, responded weakly or not at all. To determine whythe team homed in on BDNF’s receptor, a molecule called TrkB, located on the surface of cells and responsible for receiving BDNF’s chemical signals and transmitting them inside the cell. Compared with cardiac cells from mice with normal hearts, the failing heart cells had a slightly different version of the TrkB receptor, one that produces less of a catalyst protein responsible for triggering critical signaling inside the cardiac cell. This slightly sub-performing version of the receptor was less responsive to BDNF, rendering the heart cell less sensitive to it. While this TrkB variant is fairly common and does not necessarily portend disease, it may render the heart cells of those who carry the altered version less capable of using BDNF, the researchers say. Mice engineered to lack TrkB receptors in their heart cells developed impaired cardiac function. Their hearts contracted poorly, pumped blood less efficiently and took longer to relax after each beat.
“Taken together, these findings show that any abnormality in the way BDNF communicates with its receptor appears to unlock a cascade of chemical glitches that eventually leads to poor cardiac function,” Feng says.

The investigators say that disruptions in proper BDNF-TrkB signaling can even explain what drives chemotherapy-induced heart failure, a serious and well-established side effect of certain cancer treatments. Such treatments include chemicals that block multiple growth-factor receptors, TrkB among them, to halt tumor growth. And while this approach is critical to stave off cancer progression, it can also inadvertently lead to heart failure by interfering with the ability of cardiac cells to respond to the BDNF circulating in the body.
Another important finding, the researchers say, is that mice with missing BDNF receptors remained sensitive to adrenaline, the neurotransmitter released during fight-or-flight situations to infuse the heart with extra energy needed for peak cardiac performance during bouts of intense physical or emotional activity. The finding, the scientists say, means that BDNF affects cardiac function independently and separately from adrenaline by providing continuous, low-level fuel for heart contraction under normal conditions or prolonged periods of slightly elevated cardiac output, such as endurance training.
“Just like a constant low flame can keep a pot on slow simmer, constant levels of BDNF seem to maintain heart muscle vitality,” Paolocci says.  
The researchers point out that low levels of BDNF by themselves may not be enough to cause immediate heart disease, but chronic BDNF deficiency or insensitivity, compounded by additional physiologic or pathologic stressors, is a main culprit in fueling the disease.
“In the absence of chronic stressors, such as hypertension or an elevated workload of the heart muscle, BDNF deficiency may not cause full-blown disease, but it could be the proverbial straw that leads to a ‘broken heart,’” Paolocci says.
The research was funded in part by the American Heart Association under grant number GRNT17070027 and by the National Institutes of Health under grant number T32HL-0227, with additional funding support from the Magic That Matters Fund of the Division of Cardiology at Johns Hopkins.