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:

Monday, August 3, 2015

Proprioceptive Based Training for stroke recovery. Proposal of new treatment modality for rehabilitation of upper limb in neurological diseases

I would love to have a proprioception protocol, mine is still off and I know of no way to recover it. Send your doctor after the actual exercises done.
The central nervous system (CNS) has plastic properties allowing its adaptation through development. These properties are still maintained in the adult age and potentially activated in case of brain lesion.

In the present study authors hypothesized that a significant recovery of voluntary muscle contraction in post stroke patients experiencing severe upper limb paresis can be obtained, when proprioceptive based stimulations are provided. Proprioceptive based training (PBT) is based on performing concurrent movements with both unaffected and affected arm, with the aim to foster motor recovery through some mutual connections of interhemispheric and transcallosal pathways.

The aim of this pre-post pilot study was to evaluate the feasibility of PBT on recovery of voluntary muscle contraction in subacute phase after stroke.

Methods: The treatment lasted 1 h daily, 5 days per week for 3 weeks. The PBT consisted of multidirectional exercises executed synchronously with unaffected limb and verbal feedback.

The Medical Research Council scale (MRC), Dynamometer, Fugl-Meyer Upper Extremity scale (F-M UE), Functional Independence Measure scale (FIM) and modified Ashworth scale were administered at the beginning and at the end of training. Statistical significance was set at p < 0.05.

Results: Six patients with severe paresis of the upper limb within 6 months after stroke were enrolled in the study (5 ischemic and 1 hemorrhagic stroke, 3 men and 3 women, mean age 65.7 ± 8.7 years, mean distance from stroke 4.1 ± 1.5 months) and all of them well tolerated the training.

The clinical changes of voluntary muscle contraction after PBT were statistically significant at the MRC scale overall (p = 0.028), and dynamometer assessment overall (p = 0.028). Each patient improved muscle contraction of one or more muscles and in 4 out of 6 patients voluntary active movement emerged after therapy.

The functional outcomes (i.e. F-M UE and FIM) did not show significant change within group.

Conclusions: The findings of this preliminary research revealed that PBT may be a feasible intervention to improve the motricity of upper limb in stroke survivors.
Credits/Source: Archives of Physiotherapy 2015, 5:6

Study examines high costs of maintaining medical certification

I really don't give a shit about the costs. I expect my stroke doctors to be completely up-to-date on treating stroke from emergency room, through the first week of neuronal cascade of death, to specific proven rehab stroke protocols. Anything less is incompentence and should be a fireable offense from their hospitals. Somehow we have to weed out those that refuse to keep up because they are endangering our health and our recovery. As a programmer I've had to learn at least 6-8 different languages/technologies to keep up with the industry over 30+ years and I don't have other peoples lives in my hands.

National Stroke Association Advocacy: August Recess 2015 Talking Points

Failure at a gargantuan scale here.Only small scale crap here. No BHAG Big Hairy Audacious Goal at all. I don't even consider the NSA a stroke association at all, nothing they do seems to be useful for survivors.

Town Hall Talking Points (August 2015):

  • Stroke is a leading cause of long-term disability in the United States and the fifth leading cause of death.  Each year, 795,000 people experience a stroke and there are around 7 million adult stroke survivors nationwide.
  • We truly appreciate the action Congress has already taken this year to help stroke survivors. 
  • This is important to me because [personal story]
  • Of particular interest are the 21st Century Cures Act(And yet the NSA was not listed among the supporting organizations), which establishes a new tracking system for neurological diseases, and funding for the National Institutes of Health. These efforts to foster medical research into the brain are crucial to finding new ways to combat stroke.  For these reasons, I support the 21st Century Cures Act, as well as increased NIH funding and ask you to do the same.
  • Furthermore, the FAST Act (S. 1465/H.R. 2799), spearheaded by two stroke survivors in Congress, is important legislation that would help speed up the time it takes to diagnose and treat patients experiencing a stroke.  I urge you to show you support of stroke survivors around the country by co-sponsoring this bipartisan bill.
  • Thank you again for Congress’s support for the stroke community thus far, and please continue to help stroke survivors get the treatment and care they need.
  • No mention of creating a National Stroke Plan similar to the National Alzheimers Plan

Postural alignment is altered in people with chronic stroke and related to motor and functional performance

I don't give a crap about finding another stroke problem. You didn't provide ANY FUCKING SOLUTION. Damn it all, do something useful for survivors.
A great stroke association would not allow trivial stuff like this to be researched.



Trunk control is impaired after stroke but little is known about how changes in posture relate to other deficits. We examined spinal postural alignment in people with chronic stroke and explored the relationship between postural alignment and clinical measures.


Twenty-one subjects with stroke and 22 age-matched healthy comparison subjects participated in this observational, cross-sectional study. Data collection included measurements of thoracic, lumbar, sacral, and overall postural alignment in the sagittal plane in both sitting and standing. Measurements were made in different postures, including: upright, flexed forward, and extended backward. Clinical outcome measures included the Trunk Impairment Scale and its subscales, Fugl-Meyer Scale, Berg Balance Scale, Barthel Index, and Stroke Impact Scale.


Significant deviations in postural alignment for participants with stroke compared with comparison subjects were apparent in sacral alignment (P < 0.02) and overall postural alignment (P < 0.01) in standing. These measurements were also significantly correlated with clinical outcome measures poststroke. Participants with stroke who had a more forward leaning posture when upright scored worse on the coordination subscale of the Trunk Impairment Scale (r = -0.61) and Berg Balance Scale (r = -0.64). Participants with greater anterior pelvic tilt when flexed forward and more overall inclination when flexed forward and extended backward scored better on the Trunk Impairment Scale, its subscales, and Berg Balance Scale (r = -0.6-0.7).


People with chronic stroke have altered postural alignment in standing compared with subjects without neurological deficits. Investigating interventions focusing on increasing anterior and posterior pelvic tilt seem warranted.Video Abstract available. See video (Supplemental Digital Content 1, for more insights from the authors.

Views sought on Sussex stroke services

So contact them and tell them exactly where they are doing everything wrong. What are their plans to solve all the problems in stroke?
Don't let them dissemble and tell you about the processes they are doing. All we care about are results; tPA efficacy, 30 day deaths, 100% recovery. Every hospital should be required to post these results so you know which hospitals are failing stroke survivors. We don't really care about standards of care or services provided, WHAT ARE THE RESULTS OF YOUR CARE?
You have to pay it forward so future stroke survivors have an easier time of recovering than you did. And that is only possible if your hospital acknowledges that everything in stroke is a failure and needs to be worked on. Minor tweaks will not be enough, full scale tear down and rebuild of stroke services is required.

Health bosses are asking residents for their views on stroke services.

Clinical commissioning groups are working with hospital trusts and NHS providers across Sussex, the Stroke Association and South East Coast Ambulance Service as part of the Sussex Collaborative Stroke Services Review.
A spokesperson for the collaboration said: “Good progress has been made in enhancing stroke services for Sussex patients in recent years, particularly since the publication of the Department of Health’s national stroke strategy in 2007.
“However, we know there is much more we could still do to further improve outcomes for people who experience a stroke – with improvements in preventing strokes, acute stroke care and recovery.”
Dr Minesh Patel, senior responsible officer for the Sussex Collaborative Stroke Services Review, said: “Provider trusts – including local hospitals and community services – are currently developing options for how their stroke services could be improved to meet agreed national standards of care and ensure high-quality sustainable services for the future.
“Patient and carer feedback and experiences are key to ensuring we plan NHS services that work for our local community and your responses will be used to help evaluate the options that emerge.”
People are being asked for their views on prevention, admission, assessment and treatment, through to recovery and rehabilitation.
Residents can complete the survey at

Biomarker S100B Can Help Rule Out Hemorrhage After Minor Head Injury

I'm sure this won't be followed up to see if this would work for a stroke hemorrhage diagnosis, because stroke has NO strategy and the leadership in stroke is nonexistent.  If you've just had a stroke you're screwed. Maybe 50 years from now when all the fossilized leadership has died we might get somewhere.

Sunday, August 2, 2015

One step at a time: Brave Andrew Marr continues his recovery from a stroke with an outdoor workout in Primrose Hill

Stroke survivors wouldn't have to be brave if our stroke medical professionals would solve all the problems in stroke. But they won't without a change in leadership and the creation of a stroke strategy.

Bart Starr walking again after stem cell treatment

There is nothing in here that would prove that stem cell treatment caused these gains. Wishful thinking in my opinion, cause and effect has not been proven.
Bart Starr had quite a meal Tuesday morning in Alabama — three pancakes and an omelet with three eggs and cheese.
It was made by his wife Cherry, his bride of 61 years. And it didn’t take him long to eat it.
“He fed himself the entire breakfast,” Cherry Starr said. “It was great.”
It was another small but significant moment for Starr, the legendary former Green Bay Packers quarterback. Before he underwent an experimental stem cell treatment in June, Starr, 81, could barely walk or feed himself. His condition had deteriorated after suffering a heart attack, two strokes and a four seizures in September.
But now he can walk and eat unaided, seemingly sparked back to his feet with the help of this treatment.
“It’s just been really exciting to witness,” Cherry Starr told USA TODAY Sports. “Some of it might have been natural. It might have happened without the stem cells to some degree. But there’s no question that has absolutely helped him, and some of his cognition has improved rather dramatically really. He can do things like tie his shoes. He’s feeding himself. He can read. I could go on and on about a lot of things that we’re witnessing that are really, really exciting to us.”
She said Starr received an infusion of 90 million stem cells in June, when he traveled to the San Diego area for treatment. During the trip, they also met with two other sports heroes who previously received similar treatments: hockey great Gordie Howe, 87, and former San Francisco 49ers quarterback John Brodie, 79.
It was quite a moment — three iconic former athletes disabled by strokes but brought together by their faith in an experimental new medicine that has not yet been approved for widespread use in the U.S.
Brodie and Starr both were NFL MVPs and had competed against each other as recently as 1970, when Brodie led the 49ers over Starr and the Packers 26-10. Starr received his stem cell treatment the same week Howe had returned to the area for a second round of a similar treatment.
“We had a good visit when (Starr) and Gordie were here, and John was chief of enthusiasm,” John’s wife Sue Brodie told USA TODAY Sports. “I think it rubbed off on Bart, as he now has a personal trainer and has had numerous improvements. He realized that he can get better. That is the key also. He is being treated like an athlete and not a patient. Very important for these guys.”
Both Brodie and Howe received stem cell treatments at a clinic in nearby Tijuana, Mexico. Cherry Starr said she agreed not to talk about the companies and location involved in her husband’s treatment until a later time. But she described a treatment pattern similar to Brodie’s and Howe’s.
She said Bart Starr is returning to the San Diego area for more stem cells in September, this time to receive stem cells that are believed to help the brain. Similarly, Brodie and Howe received two separate injections of two different types of stem cells — mesenchymal stem cells derived from the bone marrow of an adult donor, and neural stem cells, derived from a single donated fetus. Those stem cells were manufactured by Stemedica, a company in San Diego, which didn’t return a message seeking comment about Starr.
Such a two-cell treatment is not yet available in U.S. clinical trials, but a spokesman for Stemedica previously told USA TODAY Sports that the company soon would apply to begin one in the U.S. In the meantime, its products have been tested in foreign clinical trials, including at a licensed clinic in Tijuana, where it’s less expensive to conduct.
“I think people have a strong and legitimate interest in what’s happening with stem cells, and I’ll be glad when this country will permit stem cells for the brain,” Cherry Starr said. “You shouldn’t be forced to go out of the country to receive this help.”
Experts caution that this is unproven medicine and that natural healing and physical therapy also can cause improved conditions. That’s why it’s being tested in clinical trials — to determine if it’s safe and effective. Experts also generally caution against getting unproven medicine in foreign countries because they don't have the same safety and efficacy standards as the U.S. Food and Drug Administration (FDA).
"It is understandable that patients and families facing major health issues such as strokes are looking for hope from stem cells, and I wish them the best," said Paul Knoepfler, a biomedical scientist and associate professor at the University of California, Davis. "At the same time, there is little if any evidence that these kinds of non-FDA approved treatments actually work and are safe."
On the other hand, some families just don’t feel like they have other options after a loved one suffers a debilitating stroke.
“Honestly this (condition) is the just the most undignified thing that can happen to a person,” Cherry Starr said. “It totally robs a man or a lady of their dignity.”
Cherry Starr said her husband wasn’t expected to live much longer after suffering his strokes, a sequence that started with a rare complaint of a headache. About three weeks after returning from San Diego in June, she said they started noticing significant improvements.
“This last week, he’s been walking all by himself,” she said. “It’s been pretty amazing.”
Starr spoke briefly in a video that aired in Green Bay Saturday honoring Brett Favre, another legendary quarterback who was joining him in the Packers Hall of Fame.
“Four weeks ago, he could not have done this,” Cherry Starr said. “He was able to read the teleprompter, and that was just amazing to me.”
His son, Bart Jr., spoke at the ceremony and said his father “had begun turning the corner in a significant way.”
Cherry Starr declined to say what the procedure cost. “It is an expensive procedure — that I will say,” she said. “And I’ll be glad when it’s more affordable for more people.”
She said the family has hired a therapist to work with him and is anxious for their upcoming return to the San Diego area. The two are high school sweethearts from Sidney Lanier High School in Montgomery, Ala.
“I just want a better quality of life for him, and I’ll do anything to make that happen,” she said.

A Close Look at the Connectivity of a Single Brain

If we had anything approaching a decent stroke association we could ask them for research on what connectivity looks like for stroke damaged brains. But we don't have that so we're screwed for at least another 50 years.

Where Will You Go From Here? book by Valorie Burton

5 important lessons from here. Pretty good except when she brings in God and the Bible.
1. I will not feel sorry for myself.
2. I will not stare at the closed door.
3. I will dig deep to unearth all the courage I need.
4. I will direct my thoughts - my thoughts will not direct me.
5. I will choose to believe all things work together for good.

Natural Way to Heal Nerve Damage

I wouldn't believe a single word this site writes about. There is no listed research backing up their statements. You can't trust anyone on the web including me, even though I tell you I have no medical background.
Asian Mushroom
A recommended treatment for the regeneration of nerves in the brain and spinal cord is the use of Asian mushroom, Hericium erinaceus.
 DHA, Docosahexaenoic acid
Research has shown that DHA acid, which is a component of the insulating sheath around nerve cells called myelin, is very good for healing nerve damage.
 Chanca Piedra
Chanca piedra is a tropical plant which is also known as phyllanthus in ayurvedic medicine, and quebra pedra. Though the herb is primarily used to treat diabetes, it also prevents long term complications of the central nervous system. Japanese researchers have discovered the presence of aldose reductase inhibitors in the herb which are very efficient in stopping all processes of damage in nerves.
Naturally Fermented Red Wine
Naturally fermented wines have been known to have dietary and therapeutic qualities for the past 4,000 years. (Whoopee, appeal to antiquity, bloodletting was used for hundreds of years also )

Saturday, August 1, 2015

Could a vitamin or mineral deficiency be behind your fatigue?

I have no clue and I'm sure your doctor doesn't either. But do you really think the Harvard Medical School knows how to counter stroke fatigue? Have your doctor buy this and write up a stroke protocol on fatigue.
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Does Stroke Contribute to Racial Differences in Cognitive Decline?

Genetically speaking race does not exist so this line of research doesn't really make sense. And if we had a great stroke association sponsoring research we wouldn't be wasting time and money on irrelevant questions.



It is unknown whether blacks' elevated risk of dementia is because of racial differences in acute stroke, the impact of stroke on cognitive health, or other factors. We investigated whether racial differences in cognitive decline are explained by differences in the frequency or impact of incident stroke between blacks and whites, controlling for baseline cognition.


Among 4908 black and white participants aged ≥65 years free of stroke and cognitive impairment in the nationally representative Health and Retirement Study with linked Medicare data (1998-2010), we examined longitudinal changes in global cognition (modified version of the Telephone Interview for Cognitive Status) by race, before and after adjusting for time-dependent incident stroke followed by a race-by-incident stroke interaction term, using linear mixed-effects models that included fixed effects of participant demographics, clinical factors, and cognition, and random effects for intercept and slope for time.


We identified 34 of 453 (7.5%) blacks and 300 of 4455 (6.7%) whites with incident stroke over a mean (SD) of 4.1 (1.9) years of follow-up (P=0.53). Blacks had greater cognitive decline than whites (adjusted difference in modified version of the Telephone Interview for Cognitive Status score, 1.47 points; 95% confidence interval, 1.21 to 1.73 points). With further adjustment for cumulative incidence of stroke, the black-white difference in cognitive decline persisted. Incident stroke was associated with a decrease in global cognition (1.21 points; P<0.001) corresponding to ≈7.9 years of cognitive aging. The effect of incident stroke on cognition did not statistically differ by race (P=0.52).


In this population-based cohort of older adults, incident stroke did not explain black-white differences in cognitive decline or impact cognition differently by race.

Protecting cognition from aging and Alzheimer's disease: a computerized cognitive training combined with reminiscence therapy

Would this type of therapy help stroke survivors with their cognitive problems? You'll have to figure this out yourself because nothing will be done about this in the stroke world for 50 years.



The aim of this paper was to assess the efficacy of process-based cognitive training (pb-CT) combined with reminiscence therapy (RT) in patients with mild Alzheimer's disease (mAD) and mild cognitive impairment (MCI) and in healthy elderly (HE) subjects.


This multicenter, randomized, controlled trial involved 348 participants with mAD, MCI, and HE from four European countries. Participants were randomly assigned to two arms of a crossover design: those in arm A underwent 3 months of computerized pb-CT for memory and executive functions combined with RT and 3 months of rest; those in arm B underwent the reverse. The primary outcome was the effect of the training on memory and executive functions performance. The secondary outcome was the effect of the training on functional abilities in mAD assessed with the instrumental activities of daily living.


We found a significant effect of the training for memory in all three groups on delayed recall of the Rey Auditory Verbal Learning Test and for executive functions in HE on the phonological fluency test. MCI and HE participants maintained these effects at follow-up. MCI and mAD participants also showed a significant effect of the training on the Mini-mental state examination scale. Participants with mAD showed more stable instrumental activities of daily living during the training versus the rest period.


Effect of Antibiotic Class on Stroke Outcome

In rats but it probably does mean that if you get an infection post-stroke you'll have to direct your doctor to give you the correct antibiotic. Once again, I bet this will not be followed up in human testing for 50 years because we have NO one running a stroke strategy. No one seems to give a shit about the trillions upon trillions of neurons dying every single minute worldwide.  We're flushing vast amounts of intelligence down the tube because the intelligence in our stroke associations is non-existent.



Infections are common after stroke and associated with worse outcome. Clinical trials evaluating the benefit of prophylactic antibiotics have produced mixed results. This study explores the possibility that antibiotics of different classes may differentially affect stroke outcome.


Lewis rats were subjected to transient cerebral ischemia (2 hours) and survived for 1 month. The day after stroke they were randomized to therapy with ceftiofur (a β-lactam antibiotic), enrofloxacin (a fluoroquinolone antibiotic), or vehicle (as controls) and underwent the equivalent of 7 days of treatment. Behavioral tests were performed weekly until euthanization. In a subset of animals, histology was done.


There were no differences in outcomes at 24 hours or 1 week after stroke among the different groups. At 1 month after stroke, however, performance on the rotarod was worse in enrofloxacin-treated animals when compared with control animals.


Independent of infection, the antibiotic enrofloxacin was associated with worse stroke outcome. These data echo the clinical observations to date and suggest that the secondary effects of antibiotics on stroke outcome should be considered when treating infection in subjects with stroke. The mechanism by which this antibiotic affects outcome needs to be elucidated.

Friday, July 31, 2015

pants clip fastener

Trying to close this style of pants fastener one-handed is a chore in swearing. I have just enough of a belly that I can't directly see how to line up the tab piece with the bar. So I do hit and miss sometimes for ten minutes. I'll stick to studs or buttons from now on.

Local rehab hospital earns Gold Seal of Approval - Rehabilitation Hospital of Southwest Virginia

There is absolutely nothing in here that tells me that the RESULTS are better in this hospital than other hospitals. I don't give a crap about how well you do processes. Call that hospital CEO(Georgeanne Cole, CEO) and demand to know what the RESULTS are; tPA efficacy, 30 day deaths, 100% recovery.
Big f*cking whoopee.
You can check out Joint Commission standards here:
 I saw absolutely nothing about what should be done the first week or anything about measuring 30-day deaths and 100% recovery.  God, these people are worse than worthless. Complacent good-for-nothings.

The puffery piece here:

he Rehabilitation Hospital of Southwest Virginia has earned certification for Disease-Specific Care in stroke rehabilitation. The Joint Commission’s Gold Seal of Approva was awarded to the hospital for its compliance with the organization’s national standards for healthcare quality and safety for stroke rehabilitation.
“By choosing to have The Joint Commission evaluate our stroke program, we are making a significant investment in the quality of patient care. The Joint Commission certification provides us a framework to take our hospital to the next level and helps create a culture of excellence,” said Georgeanne Cole, CEO of the Rehabilitation Hospital of Southwest Virginia. “This is a major step toward continually improving the care we provide and offering patients peace of mind knowing they are getting quality care at the industry’s highest standard.”
To earn the certification, the Rehabilitation Hospital of Southwest Virginia underwent a rigorous on-site survey on June 6, 2015. A surveyor with expertise in the care of patients with neurological issues from the Joint Commission evaluated the hospital’s stroke rehabilitation program for compliance with standards of care specific to the needs of patients and families, including the provision and quality of care, medical staff, leadership and medication management.
"In achieving Joint Commission certification, the Rehabilitation Hospital of Southwest Virginia has demonstrated its commitment to the highest level of care for its patients that suffered from a stroke," says Jean Range, M.S., R.N., C.P.H.Q., executive director, Disease-Specific Care Certification, The Joint Commission. “Certification is a voluntary process and I commend them for successfully undertaking this challenge to elevate its standard of care and instill confidence in the community it serves.”
Studies indicate that 60 percent of stroke survivors can benefit from comprehensive rehabilitation. Eighty percent of patients receiving this level of therapy return to their homes, work, schools or active retirement, according to the National Rehabilitation Caucus. The Joint Commission’s acknowledgement of the Rehabilitation Hospital of Southwest Virginia’s continuum of care for stroke offers patients and families peace of mind in knowing they are getting quality stroke care for maximized results. (But they don't say how many of their patients return to their former lives)

Stroke Care Path Primes Patients for Successful Rehabilitation - Cleveland Clinic

This really is worthless because they don't mention what the results are; tPA efficacy, 30 day deaths, 100% recovery. Cleveland Clinic should know better than to suggest that this shows how good they are.
Medium f*cking whoopee.
In 2010, Cleveland Clinic’s Neurological Institute debuted its care path for acute ischemic stroke. This guide provides comprehensive protocols for evaluation and management of patients during the acute stroke phase to help optimize patient outcomes(What are those outcomes?). It streamlines care, helps reduce hospital length of stay and ensures that every patient receives the same standard of care. Since its implementation, we have seen the Stroke Care Path benefit patients not only during the acute phases of care, but throughout their rehabilitation.
In the past few years, Cleveland Clinic has developed more than 25 care paths for other diseases and conditions, including congestive heart failure, knee and hip replacement, spine care, and dementia. All the guides are based on medical research, clinical guidelines, clinician experience and evidence collected via our Knowledge Program — a health information data collection system that gives physicians a comprehensive view of a patient’s medical status and enables researchers to broadly and quantitatively assess the effectiveness of medical decisions and processes. The Knowledge Program includes information obtained from patients by electronic questionnaires as well as clinical data extracted from Cleveland Clinic’s electronic medical record.
As we treat more patients and as medical technology advances, information in the Knowledge Program constantly evolves. So, too, must our care paths. We recently completed a revision of our Stroke Care Path to ensure that it reflects the latest evidence-based care, in addition to standards of care provided by The Joint Commission and the American Heart Association/American Stroke Association in their certification program for Primary Stroke Centers and Comprehensive Stroke Centers.

Priming Patients for Rehabilitation

Our Stroke Care Path focuses on the period from initial presentation at the emergency department or hospital with acute stroke symptoms to 90 days after hospital discharge.  The care provided during that time is paramount to successful rehabilitation. It is critically important that, as soon as patients enter the hospital, we are not only thinking about their diagnosis and treatment, but their rehabilitation. Evidence indicates that the sooner patients begin rehabilitation, the better their outcome.
Figure. Cleveland Clinic’s Neurological Institute has developed a care path for acute ischemic stroke that standardizes inpatient treatment (including for venous thromboembolism, as shown here) and rehabilitation to improve patient outcomes. ICS = Intermittent Compression Stockings EX = Enoxaparin 40mg subcutaneous daily UFH = Unfractionated Heparin 5000 units TID tPA = Tissue plasminogen activator.

By utilizing the treatment guidelines in our Stroke Care Path, physicians prepare patients for rehabilitation. The following are some of the steps we take:
  • Patients admitted with a stroke diagnosis are evaluated by a physical therapist and an occupational therapist as soon as they are medically able. This often occurs the day after admission. Patients with National Institutes of Health stroke scale scores between 4 and 20 receive a full evaluation by a physical medicine and rehabilitation physician.
  •  Nurses administer a dysphagia screen to all patients immediately upon admission unless they first require advanced procedures such as hyperacute MRI. If patients fail the swallow screening, they automatically are evaluated by a speech-language pathologist.
  •  We encourage early mobility. In the past, stroke patients often remained in bed. Now we urge them to ambulate and spend more time in a chair. We have incorporated lift devices and lift teams to help patients with limited mobility move to chairs. Early mobility has several advantages: It helps prevent urinary retention, constipation, pressure ulcers, pneumonia and deep vein thrombosis. It also is an important component of physical and occupational therapy.
  •  Patients undergo a comprehensive evaluation by a case manager within 24 hours of admission. The case manager examines all aspects of the patient’s plan of care, including finances, insurance and family/social situations. They look for anything that might prevent or limit patients’ early rehabilitation. Case managers also provide a list of rehab facilities that meet each patient’s needs and work closely with families to help select the ideal one.
  •  Each patient receives a mood screening prior to discharge and during follow-up outpatient visits. If patients suffer from poststroke depression, they are less likely to participate in their own care, thereby hindering rehabilitation efforts. Cleveland Clinic uses the Patient Health Questionnaire for Depression and Anxiety (PHQ-4) to assess mood. If patients score high, a social worker or therapist intervenes and treatment is initiated.
  •  Prior to discharge, all medications are reviewed and coordinated to reduce the risk of recurrent stroke. In addition, the discharge summary includes advice on managing personal stroke risk factors (such as blood pressure, weight and cholesterol) and a description of stroke warning signs and symptoms.

 Examining Early Urinary Catheter Removal

One recommendation in the Stroke Care Path that facilitates rehabilitation and prevents infection is removal of urinary catheters as soon as possible. However, it is important to note that the guide also cautions physicians against early removal in certain situations. They may delay removal if:
  • Patients are intermittently drowsy and unable to communicate their need to urinate
  • Patients are taking opiates, anticholinergic medications or other medications that cause obtundation or urinary retention
  • Patients are diabetic and have a history of outlet obstruction or urinary retention that predict a failed early catheter removal
  • Patients are unable to speak
In short, catheter removal requires that patients are adequately alert and physically able to say when they need to use the bathroom.

Guiding Informed Decisions

The Stroke Care Path is an invaluable tool for our physicians to provide evidence-based poststroke care(Not Results) and prepare patients for successful rehabilitation. It is used not only within Cleveland Clinic hospitals, but in ambulatory therapy centers and subacute and rehabilitation facilities. This allows us to implement best practices and a high standard of care through the entire course of our patients’ medical and rehabilitative treatment.

Curing cancer in 10 years: Is it hype? And is that hype OK?

We've got goals for cancer and Alzheimers but nothing for stroke. Leadership failure of our stroke associations on every level. With no goal or plan for stroke solutions we will continue to flounder and trillions upon trillions of neurons will needlessly die.
Once again, we have jackshit leaders, WAITING FOR SOMEONE ELSE TO SOLVE THE PROBLEM
The problem is; 'How do you get to 100% recovery?' It's a simple question. Solve the hard answer.

Curing cancer in 10 years: Is it hype? And is that hype OK?

The goal of National Alzheimer's Plan to prevent and effectively treat Alzheimer's by 2025.

My high blood pressure

Yesterday I was planning on giving blood again. Got there, took my blood pressure,186/98. Never been higher than 140/88. The cutoff for donating is 180 so I'll have to do it another time.
I will not be taking any blood pressure medications. If I need to I'll use beet juice and watermelon juice to lower it. DO NOT follow my ideas, you can ask your doctor but I'll guarantee they will know nothing about more natural ways to reduce blood pressure.

Bach1 Represses Wnt/β-Catenin Signaling and Angiogenesis

Since we would like to have angiogenesis what is your doctor doing to reduce Bach1?

  1. Dan Meng
+ Author Affiliations
  1. From the Department of Physiology and Pathophysiology (L.J., Xiangxiang Wei, J.L., Xinhong Wang, C.N., X.K., J.X., Z.Z., R.Q., N.S., A.C., R.W., S.C., D.M.) and Department of Biochemistry and Molecular Biology (S.S., Xu Wang), School of Basic Medical Sciences, Fudan University, Shanghai, China; Department of Cardiothoracic Surgery, Shanghai Children’s Medical Center, Shanghai Jiao Tong University School of Medicine, Shanghai, China (M.Y.); Key Laboratory of Nutrition and Metabolism, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, China (X.Z., S.D.); Department of Cardiology, Shanghai Institute of Cardiovascular Disease, ZhongShan Hospital, Fudan University, Shanghai, China (K.Y.); Center for Vascular Disease and Translational Medicine, Xiangya Third Hospital, Central South University, Changsha, China (A.C.); Department of Biology, Laurentian University, Sudbury, Ontario, Canada (R.W.); and Division of Cardiology, Department of Medicine, Stem Cell Institute, University of Minnesota Medical School, Minneapolis (J.Z.).
  1. Correspondence to Dan Meng, MD, or Sifeng Chen, MD, Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Fudan University, 138 Yixueyuan Rd, PO Box 224, Shanghai 200032, China. E-mails or
  1. * These authors contributed equally to this article.


Rationale: Wnt/β-catenin signaling has an important role in the angiogenic activity of endothelial cells (ECs). Bach1 is a transcription factor and is expressed in ECs, but whether Bach1 regulates angiogenesis is unknown.
Objective: This study evaluated the role of Bach1 in angiogenesis and Wnt/β-catenin signaling.
Methods and Results: Hind-limb ischemia was surgically induced in Bach1–/– mice and their wild-type littermates and in C57BL/6J mice treated with adenoviruses coding for Bach1 or GFP. Lack of Bach1 expression was associated with significant increases in perfusion and vascular density and in the expression of proangiogenic cytokines in the ischemic hindlimb of mice, with enhancement of the angiogenic activity of ECs (eg, tube formation, migration, and proliferation). Bach1 overexpression impaired angiogenesis in mice with hind-limb ischemia and inhibited Wnt3a-stimulated angiogenic response and the expression of Wnt/β-catenin target genes, such as interleukin-8 and vascular endothelial growth factor, in human umbilical vein ECs. Interleukin-8 and vascular endothelial growth factor were responsible for the antiangiogenic response of Bach1. Immunoprecipitation and GST pull-down assessments indicated that Bach1 binds directly to TCF4 and reduces the interaction of β-catenin with TCF4. Bach1 overexpression reduces the interaction between p300/CBP and β-catenin, as well as β-catenin acetylation, and chromatin immunoprecipitation experiments confirmed that Bach1 occupies the TCF4-binding site of the interleukin-8 promoter and recruits histone deacetylase 1 to the interleukin-8 promoter in human umbilical vein ECs.
Conclusions: Bach1 suppresses angiogenesis after ischemic injury and impairs Wnt/β-catenin signaling by disrupting the interaction between β-catenin and TCF4 and by recruiting histone deacetylase 1 to the promoter of TCF4-targeted genes.

Stroke services at James Cook highly rated by national audit - Middlesbrough, United Kingdom

This means absolutely nothing. Getting assessed and seem by staff in a particular time means nothing. You have to look at the results - tPA efficacy, 30 day deaths, 100% recovery.  People who tout this really shouldn't even consider themselves a stroke unit.

EIGHT out of ten patients are reaching the stroke unit at James Cook University Hospital, Middlesbrough, within four hours of arrival, compared to five out of ten nationally.
The data, released by the Royal Collage of Physicians’ Sentinel Stroke National Audit Programme, also reveals that the average patient arrives on the stroke ward within 90 minutes following initial assessments and routine scans.
Figures show South Tees Hospitals NHS Foundation Trust was the only service in the country to achieve more than 90 per cent of patients seeing a stroke nurse and stroke therapist within 24 hours - and all relevant therapists within 72 hours.
The proportion of applicable patients receiving six month reviews at 89 per cent - is also well above the national average of 21 per cent.
Stroke consultant Dr Adrian Bergin said: “What these statistics show is that we get patients to the right place quickly and assessed by the right people.”
The figures are expected to improve even further in the future following the opening of the specialist stroke rehabilitation unit at Redcar Primary Care Hospital in April and the launch of the early supported discharge (ESD) team, which now enables up to 40 per cent of South Tees patients to receive stroke rehabilitation therapy in their own home.
Dr Ali Tahmassebi, South Tees Clinical Commissioning Group GP and lead for the IMProVE programme (Integrated Management and Proactive Care for the Vulnerable and Elderly) behind the positive changes to stroke services, said: “We are delighted to receive further confirmation that James Cook continues to improve stroke care.” (Not results)

Thursday, July 30, 2015

Blood test predicts prognosis for traumatic brain injuries

Another possibility that needs more followup research to see if this would work for stroke. Who the hell do we talk to to get this accomplished? Or do we just sit and wait 50 years because we have no stroke leaders or any strategy to fix stroke problems?

A new blood test could help emergency room doctors quickly diagnose traumatic brain injury and determine its severity. The findings, published July 10 in the Journal of Neurotrauma, could help identify patients who might benefit from extra therapy or experimental treatments.
"Compared to other proteins that have been measured in , BDNF does a much better job of predicting outcomes," says Frederick Korley, M.D., Ph.D., an assistant professor of emergency medicine at the Johns Hopkins University School of Medicine and first author of the new paper.
After a hit to the head or rapid whiplash, whether from a car crash, athletic event or other accident, millions of Americans develop traumatic brain injuries (TBIs) each year. TBIs can range from mild concussions—causing only a headache or temporary blurred vision—to much more severe injuries—causing seizures, confusion, memory and attention problems, muscle weakness, or coma for many months. These symptoms, whether mild or more severe, are generally caused by damaged brain cells.
Until now, most physicians have relied on CT scans and patients' symptoms to determine whether to send them home and have them resume their usual activities or take extra precautions. However, CT scans can only detect bleeding in the brain, not damage to brain cells, which can happen without bleeding.
"A typical situation is that someone comes to the emergency department with a suspected TBI, we get a CT scan, and if the scan shows no bleeding, we send the patient home," says Korley. "However, these patients go home and continue having headaches, difficulty concentrating and memory problems, and they can't figure out why they are having these symptoms after doctors told them everything was fine."
Korley and collaborators around the country wanted to know if a blood test could better predict which patients would have ongoing brain injury-related problems, to provide better treatment for them. So they measured the levels of three proteins that they suspected play a role in brain cell activity in more than 300 patients with a TBI and 150 patients without brain injuries. Then, they followed those with a TBI for the next six months.
Levels of one protein, called brain-derived neurotrophic factor (BDNF), taken within 24 hours of someone's head injury, could predict the severity of a TBI and how a patient would fare, they found. While healthy people averaged 60 nanograms per milliliter of BDNF in their bloodstreams, patients with brain injuries had less than one-third of that amount, averaging less than 20 nanograms per milliliter, and those with the most severe TBIs had even lower levels, around 4 nanograms per milliliter. Moreover, patients with high levels of BDNF had mostly recovered from their injuries six months later. But in patients with the lowest levels of BDNF, symptoms still lingered at follow-up. The results suggest that a test for BDNF levels, administered in the emergency room, could help stratify patients.
"The advantage of being able to predict prognosis early on is that you can advise patients on what to do, recommend whether they need to take time off work or school, and decide whether they need to follow up with a rehab doctor or neurologist," Korley says. In addition, it could help decide which to enroll in clinical trials for new drugs or therapies targeting severe TBIs.
Korley would like to follow up with more research on why, at a molecular level, brain injuries lower levels of BDNF in the blood and whether things known to increase BDNF levels—including exercise and omega-3 fatty acids—could help treat TBIs. He also wants to know whether changes in BDNF levels over time can be a proxy for recovery and if they could be used to gauge the effectiveness of an intervention.
"We looked at that very first blood sample obtained within 24 hours of an injury," he says. "But for BDNF to be used as a surrogate outcome, we'll have to see what happens to BDNF blood levels down the line, at one, three or six months after the injury." He and his collaborators have already started collecting data for those prospective studies, he adds.
Journal reference: Journal of Neurotrauma search and more info

Experience with the “Good” Limb Induces Aberrant Synaptic Plasticity in the Perilesion Cortex after Stroke

Well if using the 'good' side impairs recovery of the 'bad' side then all survivors are totally fucking screwed in trying to get 100% recovery.  Which to me means we need to stop a lot of the damage in the first place by stopping the neuronal cascade of death.
What is your doctors solution to get around this problem? I don't know is not an ok answer.
  1. Theresa A. Jones2,3
  1. Author contributions: S.Y.K., R.P.A., D.L.A., J.A.K., and T.A.J. designed research; S.Y.K., R.P.A., D.L.A., K.A.T., N.A.D., and T.A.J. performed research; J.A.K. contributed unpublished reagents/analytic tools; S.Y.K., R.P.A., D.L.A., and T.A.J. analyzed data; S.Y.K. and T.A.J. wrote the paper.
  2. *R.P.A. and D.L.A. contributed equally to this work.
  1. The Journal of Neuroscience, 35(22): 8604-8610; doi: 10.1523/JNEUROSCI.0829-15.2015


Following unilateral stroke, the contralateral (paretic) body side is often severely impaired, and individuals naturally learn to rely more on the nonparetic body side, which involves learning new skills with it. Such compensatory hyper-reliance on the “good” body side, however, can limit functional improvements of the paretic side. In rats, motor skill training with the nonparetic forelimb (NPT) following a unilateral infarct lessens the efficacy of rehabilitative training, and reduces neuronal activation in perilesion motor cortex. However, the underlying mechanisms remain unclear. In the present study, we investigated how forelimb movement representations and synaptic restructuring in perilesion motor cortex respond to NPT and their relationship with behavioral outcomes. Forelimb representations were diminished as a result of NPT, as revealed with intracortical microstimulation mapping. Using transmission electron microscopy and stereological analyses, we found that densities of axodendritic synapses, especially axo-spinous synapses, as well as multiple synaptic boutons were increased in the perilesion cortex by NPT. The synaptic density was negatively correlated with the functional outcome of the paretic limb, as revealed in reaching performance. Furthermore, in animals with NPT, there was dissociation between astrocytic morphological features and axo-spinous synaptic density in perilesion motor cortex, compared with controls. These findings demonstrate that skill learning with the nonparetic limb following unilateral brain damage results in aberrant synaptogenesis, potentially of transcallosal projections, and this seems to hamper the functionality of the perilesion motor cortex and the paretic forelimb.

Augmentation of M-Type (KCNQ) Potassium Channels as a Novel Strategy to Reduce Stroke-Induced Brain Injury

Another possibility that needs more followup research. Who the hell do we talk to to get this accomplished? Or do we just sit and wait 50 years because we have no stroke leaders or any strategy to fix stroke problems?
  1. Mark S. Shapiro1
  1. Author contributions: S.M.B., J.D.L., and M.S.S. designed research; S.M.B. performed research; S.M.B., F.S.C., J.D.L., and M.S.S. contributed unpublished reagents/analytic tools; S.M.B. and F.S.C. analyzed data; S.M.B. and M.S.S. wrote the paper.
  1. The Journal of Neuroscience, 35(5): 2101-2111; doi: 10.1523/JNEUROSCI.3805-14.2015


Cerebral ischemic stroke is a worldwide cause of mortality/morbidity and thus an important focus of research to decrease the severity of brain injury. Therapeutic options for acute stroke are still limited. In neurons throughout the brain, “M-type” K+ currents, underlain by KCNQ subunits 2–5, play dominant roles in control over excitability, and are thus implicated in myriad neurological and psychiatric disorders. Although KCNQ channel openers, such as retigabine, have emerged as anti-epilepsy drugs, their effects on ischemic injury remain unknown. Here, we investigated the protective effects of M-channel openers on stroke-induced brain injury in mouse photothrombotic and middle cerebral artery occlusion (MCAo) models. Both photothrombosis and MCAo led to rapid, predictable, and consistently sized necrotic brain lesions, inflammatory responses, and behavioral deficits. Administration of three distinct M-channel openers at 0–6 h after ischemic injury significantly decreased brain infarct size and inflammation, and prevented neurological dysfunction, although they were more effective when administered 0–3 h poststroke. Thus, we show beneficial effects against stroke-induced brain injury and neuronal death through pharmacological regulation of ion channels that control neuronal excitability.

B-Lymphocyte-Mediated Delayed Cognitive Impairment following Stroke

With double the risk of dementia post-stroke your doctor better have a protocol to prevent that. But I bet s/he does not have anything at all. You're screwed.
  1. Marion S. Buckwalter1,6
  1. Author contributions: K.P.D., L.N.Q., M.S., R.C.A., T.V.V.N., GJ..S.-L., S.J., J.H., L.S., F.M.L., J.A.S., R.C.M., and M.S.B. designed research; K.P.D., L.N.Q., M.S., R.C.A., T.V.V.N., G.J.S.-L., S.J., and J.H. performed research; J.A.S. contributed unpublished reagents/analytic tools; K.P.D., R.C.M., and M.S.B. analyzed data; K.P.D., J.A.S., and M.S.B. wrote the paper.
  1. The Journal of Neuroscience, 35(5): 2133-2145; doi: 10.1523/JNEUROSCI.4098-14.2015


Each year, 10 million people worldwide survive the neurologic injury associated with a stroke. Importantly, stroke survivors have more than twice the risk of subsequently developing dementia compared with people who have never had a stroke. The link between stroke and the later development of dementia is not understood. There are reports of oligoclonal bands in the CSF of stroke patients, suggesting that in some people a B-lymphocyte response to stroke may occur in the CNS. Therefore, we tested the hypothesis that a B-lymphocyte response to stroke could contribute to the onset of dementia. We discovered that, in mouse models, activated B-lymphocytes infiltrate infarcted tissue in the weeks after stroke. B-lymphocytes undergo isotype switching, and IgM, IgG, and IgA antibodies are found in the neuropil adjacent to the lesion. Concurrently, mice develop delayed deficits in LTP and cognition. Genetic deficiency, and the pharmacologic ablation of B-lymphocytes using an anti-CD20 antibody, prevents the appearance of delayed cognitive deficits. Furthermore, immunostaining of human postmortem tissue revealed that a B-lymphocyte response to stroke also occurs in the brain of some people with stroke and dementia. These data suggest that some stroke patients may develop a B-lymphocyte response to stroke that contributes to dementia, and is potentially treatable with FDA-approved drugs that target B cells.