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

What this blog is for:

Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.
My back ground story is here:

Monday, December 10, 2018

Two Compounds in Coffee May Team Up to Fight Parkinson's

Is this enough to get your stroke hospital to finally create a 24 hour coffee station? Or will they DO NOTHING?   Or will they wait for SOMEONE ELSE TO SOLVE THE PROBLEM?

I want to know if my 8-10 cups of coffee a day is enough. Simple question.

Your risk of getting Parkinsons here:

Parkinson’s Disease May Have Link to Stroke


Two Compounds in Coffee May Team Up to Fight Parkinson's

Mon, 12/10/2018 - 2:39pm
by Rutgers University
M. Maral Mouradian of Rutgers Robert Wood Johnson Medical School has found a compound in coffee that when paired with caffiene may help to fight Parkinson's disease and Lewy body dementia. Credit: Steve Hockstein/Harvard Studio
Rutgers scientists have found a compound in coffee that may team up with caffeine to fight Parkinson's disease and Lewy body dementia - two progressive and currently incurable diseases associated with brain degeneration.
The discovery, recently published in the Proceedings of the National Academy of Sciences, suggests these two compounds combined may become a therapeutic option to slow brain degeneration.
Lead author M. Maral Mouradian, director of the Rutgers Robert Wood Johnson Medical School Institute for Neurological Therapeutics and William Dow Lovett Professor of Neurology, said prior research has shown that drinking coffee may reduce the risk of developing Parkinson's disease. While caffeine has traditionally been credited as coffee's special protective agent, coffee beans contain more than a thousand other compounds that are less well known.
The Rutgers study focused on a fatty acid derivative of the neurotransmitter serotonin, called EHT (Eicosanoyl-5-hydroxytryptamide), found in the bean's waxy coating. The researchers found that EHT protects the brains of mice against abnormal protein accumulation associated with Parkinson's disease and Lewy body dementia.
In the current research, Mouradian's team asked whether EHT and caffeine could work together for even greater brain protection. They gave mice small doses of caffeine or EHT separately as well as together. Each compound alone was not effective, but when given together they boosted the activity of a catalyst that helps prevent the accumulation of harmful proteins in the brain. This suggests the combination of EHT and caffeine may be able to slow or stop the progression of these diseases. Current treatments address only the symptoms of Parkinson's disease but do not protect against brain degeneration.
Mouradian said further research is needed to determine the proper amounts and ratio of EHT and caffeine required for the protective effect in people.
"EHT is a compound found in various types of coffee but the amount varies. It is important that the appropriate amount and ratio be determined so people don't over-caffeinate themselves, as that can have negative health consequences," she said.
According to the U.S. Department of Health & Human Services, Parkinson's disease is a brain disorder that can lead to shaking, stiffness and difficulty with walking, balance and coordination. Nearly one million people in the United States are living with Parkinson's disease. Lewy body dementia, one of the most common forms of dementia, affects more than one million people in the United States. It causes problems with thinking, behavior, mood, and movement.

Hospital named primary stroke care center, Sentara Albemarle Medical Center, Elizabeth city, NC

And just why the fuck should we go to a 'care' center rather than a 'results' center? If you can't tell us your results you are hiding how fucking bad they are. We have to completely change how stroke is discussed, every single article on stroke should be mentioning exactly what the failures are and what is being done to fix them.   Notice they don't tell us;

  1. tPA full recovery better than 12%?

  2. Full stroke recovery better than 10%?

  3.  30 day stroke deaths better than your competitors?


Hospital named primary stroke care center, Sentara Albemarle Medical Center,  Elizabeth city, NC

An international quality assurance and accreditation firm has recognized Sentara Albemarle Medical Center for its management of stroke patients by designating the hospital a Primary Stroke Center.
DNV GL Healthcare, a branch of Norway-based DNV GL, certified Sentara Albemarle as a Primary Stroke Center following an on-site review in September, the hospital announced recently. According to Sentara, it's the first time the hospital, formerly known as Albemarle Hospital, has won the distinction in its 104-year history.
The certification validates the hospital's abilities, but also shows providers and staff are dedicated to high-quality health care for northeastern North Carolina, Sentara President Coleen Santa Ana said in the release.
“Attaining a certification of this magnitude required commitment from across the entire hospital to develop and execute a new program, and we will continue to aim toward the highest levels of performance,” Santa Anna said in the release.
There are several key steps the hospital has taken to improve stroke care since 2016, the release explains. It implemented “tele-stroke technology” that allows quick contact between a patient and a neurologists, as well as new stroke protocols and training to provide a rapid, hospitalwide response to patients showing signs of a stroke. That allows a “stroke alert team” to immediately provide care, the hospital said.
Additionally, the hospital has worked to diagnose ischemic strokes — strokes caused by blood clots or otherwise reduced blood flow to the brain — and provide a “clot-busting” medication within an hour of a patient's arrival at the hospital. The American Stroke Association recommends that standard, the hospital said.
Sentara Albemarle also has added a nurse practitioner and stroke coordinator to the hospital's work force, and partnered closely with Pasquotank-Camden Emergency Medical Services to streamline care for stroke patients transported by the ambulance service.
In Sentara’s release, EMS Director Jerry Newell offers his “kudos” to the hospital, noting EMS and Sentara Albemarle have worked to deliver “big-town stroke care at our community hospital.”
The release notes that the Primary Stroke Center designation is the second-highest of three stroke certifications DNV-GL can award. The lowest level is Acute Stroke Ready, which can help stabilize patients for transport. Primary Stroke Centers can manage stroke patients' care and only need to transport them for “neurosurgical emergencies.”
The highest-level certification is Comprehensive Stroke Center, which applies to hospitals that provide the most advanced stroke care. The closest Comprehensive Stroke Center to Sentara Albemarle is Sentara Norfolk General Hospital, according to Sentara’s release.
The certifications are also based on standards set by the American Stroke Association and Brain Attack Coalition, the release notes.
In a follow-up email, Sentara Albemarle spokeswoman Annya Soucy said the hospital isn’t seeking to become a Comprehensive Stroke Center, but will continue working to improve care for stroke patients.
The hospital’s initiatives include speeding up administration of an anti-clotting medication and teaching community members a mnemonic device, “BEFAST,” for spotting strokes. BEFAST refers to monitoring for impairment to a person’s balance, eyes, face, arms, speech, and the time that has elapsed since the person’s normal functioning.
Citing statistics from the National Stroke Association and the N.C. Stroke Association, Sentara Albemarle’s release said strokes kill nearly 130,000 people nationwide every year. Coastal North Carolina is also part of the “stroke buckle” where the death rate from strokes is “twice the national average,” the release adds.

Weeks after stroke, editor Bob Gabordi: 'I just want to be who I was. I want to go home'

So your doctor is not being honest with you about your 10% chance of full recovery. Or not telling you there are NO stroke rehab protocols. Lying by omission? 

Weeks after stroke, editor Bob Gabordi: 'I just want to be who I was. I want to go home'

One day, during physical therapy, I noticed a small Christmas tree. It wasn’t much of a tree, really. But it had my attention, like a mirage in the desert.
I’m rehabilitating from a Nov. 9 stroke at Sea Pines Rehabilitation Hospital in Palm Bay, after lifesaving stops at Viera Hospital and Cape Canaveral Hospital.
Sea Pines is an amazing, wonderful place that restores the “people-ness” to people with broken bodies like mine. Honestly, so many have it worse — face more difficult obstacles — than me.
Some days are better than others. My problem is that I judge my progress and potential based on my latest therapy session. Some days I’m way ahead of everyone’s expectations — except mine, of course. Everyone says I should give myself some credit, or a break. But I don’t want either. I just want to be who I was before the stroke, and I want to go home.

Neurofilament Light Protein Tied to Cognitive Decline

Don't just lazily describe a problem and not give any solution. 

Neurofilament Light Protein Tied to Cognitive Decline

  • by Contributing Writer, MedPage Today
Neurofilament light protein levels in cerebrospinal fluid (CSF) were tied to cognitive impairment in dementia patients and neurodegeneration intensity in other disorders, researchers reported.
And adding it to a three-biomarker panel -- consisting of 42-residue amyloid beta protein (AB-42), total tau, and phosphorylated tau -- improved its ability to discriminate among certain neurodegenerative disorders for which the differential diagnosis is often difficult, according to Bob Olsson, MD, PhD, of the University of Gothenburg in Sweden, and co-authors, in JAMA Neurology.
"Neurofilament light levels reflect cognitive dysfunction in patients with Alzheimer's disease and frontotemporal dementia (FTD)," Olsson told MedPage Today. "It may help to separate different forms of neurodegenerative diseases from each other and cognitive decline from other causes than neurodegeneration, such as depression or drug-related side effects."
Neurofilament light protein previously has been shown to be elevated in different forms of dementia and amyotrophic lateral sclerosis (ALS). Although other studies have shown similar findings, "this study is the most exhaustive to date and includes a much larger sample size and a wider range of neurodegenerative diseases to compare CSF neurofilament light levels," noted Michelle Mielke, PhD, of the Mayo Clinic in Rochester, Minnesota, who was not involved with the study.
"It is notable that the addition of CSF neurofilament light to CSF amyloid-beta, total tau, and phosphorylated tau greatly increased the accuracy of distinguishing ALS or FTD patients compared to controls," Mielke told MedPage Today. "However, it is not yet clear how much the addition of CSF neurofilament light to the other CSF biomarkers will help with differentially diagnosing the specific type of neurodegenerative disease."
In this study, Olsson and co-authors analyzed neurofilament light levels in CSF samples from 913 people with an average age of about 69. The group included 75 healthy controls and 845 patients with clinical diagnoses of neurodegenerative disorders including mild cognitive impairment (n=114), Alzheimer's disease (n=397), FTD (n=96), ALS (n=68), Parkinson's disease (n=41), Parkinson's disease with mild cognitive impairment (n=19), Parkinson's disease with dementia (n=29), dementia with Lewy bodies (n=33), corticobasal syndrome (n=21), and progressive supranuclear palsy (n=20).
Mini-Mental State Examination (MMSE) scores were analyzed every 6 months for most patients, and autopsy-verified diagnoses were available for 120 of the 845 patients with diseases.
Neurofilament light levels were elevated in a stepwise manner, with the lowest levels in control participants, significantly higher levels in patients with mild cognitive impairment, and even higher levels in Alzheimer's disease. Although the highest levels were observed in patients with ALS and the second-highest levels in those with FTD, neurofilament light concentrations were elevated in Parkinson's disease with dementia, dementia with Lewy bodies, corticobasal syndrome, and progressive supranuclear palsy patients, compared with controls.
Neurofilament light levels rose with increasing cognitive impairment, with higher levels in Alzheimer's patients, intermediary levels in patients with mild cognitive impairment, and lowest levels in controls. They correlated significantly with annual worsening in cognitive performance on MMSE in patients with Alzheimer's or FTD, but not in patients with mild cognitive impairment. They also were tied to the severity of transactive response DNA-binding protein-43 in 13 of 17 brain regions.
Adding neurofilament light to the three-biomarker panel of AB-42, total tau, and phosphorylated tau led to:
  • 29% (95% CI 25.0%-33.3%) increase in accuracy in distinguishing between controls and ALS, from 62% to 91%
  • 17% (95% CI 14.9%-19.5%) increase between controls and the behavioral variant of FTD, from 63% to 81%
  • 14% (95% CI 8.7%-19.1%) increase between Parkinson's disease and progressive supranuclear palsy, from 62% to 76%
"Future studies with serially-collected samples across the neurodegenerative diseases will be useful for understanding how CSF neurofilament light tracks with the progression of each disease," noted Mielke.
The study has a number of limitations: some subgroups have small sample sizes, and the risk of false-positive statistical test results warrants replication of the findings, the authors noted. While the MMSE is not a strong indicator of disease severity for FTD, it was the only measure of cognition available for all FTD patients.
The study was supported by grants from the Swedish and European Research Councils, the Torsten Söderberg Foundation, the Swedish Brain Foundation, the Knut and Alice Wallenberg Foundation, Frimurarestiftelsen, Stiftelsen för Gamla Tjänarinnor, Foundation for Research on Alzheimer, the Swedish Alzheimer Foundation, and Swedish State Support for Clinical Research in addition to the National Institutes of Health.
Researchers reported relationships with Merck, Biogen, Avid Radiopharmaceuticals, Eli Lilly, GE Healthcare, Janssen, Brain Biomarker Solutions, Roche Diagnostics, Teva, Alzheon, BioArctic, Fujirebio Europe, IBL International, and Pfizer.
last updated

Plasma CLEC-2 (C-Type Lectin Receptor 2) in Patients With Acute Ischemic Stroke

Shit, once again using the subjective and no discrimination Rankin scale as an endpoint.  I got nothing out of this because it talks about risk markers NOT anything to do with recovery. USELESS.

Plasma CLEC-2 (C-Type Lectin Receptor 2) in Patients With Acute Ischemic Stroke

You'll have to read at link, copying and reformatting is not my job, that is your doctors job. 

Advanced Software Allows Later Stroke Treatment

So once again you need to have the perfect stroke to be treated, nothing here about getting patients 100% recovered. That is the only goal, not faster treatment or better results. 100% recovery. GET THERE!

Advanced Software Allows Later Stroke Treatment

The treatment of stroke patients has been characterized by the need for speed. The only medical therapy available, a clot dissolving drug called tPA, was originally available for use only if it could be given less than 3 hours after the start of symptoms. This led to the development of stroke centers to treat patients as rapidly as possible. Ten years ago the time was extended to 4.5 hours for some patients.

In recent years, another type of stroke treatment has been developed known as endovascular thrombectomy. In this procedure, a catheter is guided into a brain artery, and a device is used to pull a clot out of the brain. In 2015, this procedure was demonstrated to benefit patients with the most severe strokes, those due to large clots, up to 6 hours after the start of symptoms.

Researchers have been working for years to find a way to identify patients who would benefit from later treatment. These patients, who are suffering a stroke due to a lack of blood flow to the brain, are those who have not yet suffered significant damage. 

A breakthrough advance in the selection of stroke patients for therapy is  software that is able to analyze special CT scan images, known as CT perfusion. This software can automatically determine which patients have a small area of permanent damage, and an area that can be potentially saved by available treatments.

Using one type of software, known as RAPID, it has now been demonstrated in multiple stroke studies performed around the world that some patients may be treated with thrombectomy up to 24 hours. Only during the past month researchers from Australia showed that using this software, some patients can be successfuly treated with tPA (Your definition of success is appalling, I expect success to be 100% recovery. When the hell are you going to deliver that success?)up to 9 hours following the beginning of stroke symptoms.
As this software, and others like it, come into more common use, more stroke patients will be treated later and more effectively.
Thrombectomy is being performed up to 24 hours in many stroke centers, and in the future, the window for tPA is expected to be extended.

Silk Biomaterial Could Regenerate the Brain After a Stroke

WHOM DO OUR DOCTORS AND STROKE HOSPITAL CONTACT TO GET THIS RESEARCH DONE? Specific names please so we can ding them to make sure followup was done.


Silk Biomaterial Could Regenerate the Brain After a Stroke

A group of researchers in Spain has developed a silk biomaterial that can increase the survival of transplanted stem cells into the brain, improving recovery after a stroke or brain injury.
The nervous system has limited capacity to recover after an injury, such as those produced by a stroke or brain trauma. Stem cell transplants are a promising therapy to promote regeneration of the brain by reducing the extent of the damage and promoting the remodeling of the brain. However, most of the cells don’t survive the procedure due to the inflammatory environment created in the brain after an injury.
A study has shown that encapsulating stem cells into a biomaterial containing silk proteins could protect the cells and make them last significantly longer when treating stroke in mice.

“In many cell therapy studies, most of the mesenchymal stem cells implanted don’t survive beyond 1-2 weeks after the implantation,” Daniel Gonzalez-Nieto, researcher at the Polytechnic University of Madrid (UPM), told me. “In this study we found that our biomaterial increases the survival of these cells in the brain to over 4 weeks.”
With more cells surviving the procedure, the mice recovered better. “The changes were extraordinary, the treatment improved the sensory and movement ability of the animals that had suffered a stroke,” said Gonzalez-Nieto.
The encapsulated stem cells were able to reduce the size of the lesion and promote the remodeling of the brain areas adjacent to the injury, making the neurons take over control of the functions that were lost after the stroke.
“This remodeling around the lesion has been observed in patients that improve after a stroke or some type of brain trauma,” explained Gonzalez-Nieto. “These patients are a minority and they get better because the damaged area is smaller and respond relatively better to physical rehabilitation.”
silk fibroin biomaterial stroke stem cells
The biomaterial consists of a hydrogel containing silk fibroin, a protein that the researchers extracted from the silk of the cocoons of the silkworm. According to Gonzalez-Nieto, the material has been used for decades in medical practice for applications such as wound stitching.
Compared to other biomaterials, silk fibroin does not generate any immune response against it. In addition, silk fibroin doesn’t produce any toxic by-products when it degrades, as is the case with hyaluronic acid, a biomaterial commonly used in research to encapsulate cells and drugs.
Silk has indeed become a popular biomaterial in medical biotech applications. In Italy, the company Silk Biomaterials is also developing silk scaffolds to repair damage in peripheral nerves. Silk proteins are also being used to create stronger vaccines.
The goal now is to get the biomaterial ready to start clinical trials in humans in collaboration with Silk Biomed. A spin-off of the UPM, the company was founded in 2016 with a €1M grant with the goal of developing clinical applications for this biomaterials.
“Before starting clinical trials we need to determine the optimal time point to administer the therapy and the number of cells needed to maximize the beneficial effects of the therapy. We’re running different tests in vitro and in vivo and we expect that in 2019 we’ll be able to obtain a pharmaceutical product that is safe and suitable to treat brain injury,” Fivos Panetsos, co-founder and CEO of Silk Biomed, told me.
The applications of this silk biomaterial go beyond stroke and brain injury. Panetsos explained that the company is also looking into developing and testing biomaterials for neurodegenerative diseases such as Parkinson’s and Alzheimer’s, eye diseases like glaucoma and age-related macular degeneration, the repair of skin and tendons, and the treatment of incontinence and impotence caused by prostate surgery. 

Oxford neurologist's stroke turned his life upside down

One sentence in here is instructive. Your doctors and therapists will never understand stroke survivors unless they have a stroke. "I want people to know that one can work in the field of brain injury for decades and yet not fully understand what survivors are going through." This is precisely why stroke survivors need to be in charge of stroke associations and stroke research.

Oxford neurologist's stroke turned his life upside down

A NEUROLOGIST who spent 20 years improving the lives of brain injury survivors, despite also dealing with the effects of his own stroke, has been shortlisted for a national award.
Professor Udo Kischka, 64, has helped improve the lives of countless brain injury patients while working as a Neuro Rehabilitation Consultant at the Oxford Centre of Enablement since 2004.
Realising the lack of community support available for some brain injury survivors, he helped to foster stronger ties between the OCE and Headway Oxfordshire, eventually volunteering to join the charity's board of trustees.
However, the father-of-two’s life was changed forever after he himself suffered a stroke while running for a train in 2016.
Speaking about the life-altering event, he said: "Theoretically, I knew I should seek medical attention but I didn't.
"Because of the bleed in my brain I felt unnaturally calm. If that happened to someone else I would tell them to go to hospital straight away.
"It's difficult looking back on that. It wasn't clever, but that's what my brain injury did to me."
At home he didn't tell his wife Helen about what happened and carried on working at his desk, eventually slipping into unconsciousness in the early hours of the morning.
He came round lying on the floor of his study, unable to move the left side of his body.
He said: “It was truly terrifying - I couldn’t move and couldn’t shout out."
The professor's wife found him some hours later and he was rushed to the John Radcliffe Hospital.
When he was discharged nine months later, Prof Kischka became involved with Headway Oxfordshire once more, but this time, as a service user.
Throughout his recovery, Prof Kischka says he developed a far deeper understanding of stroke rehabilitation becoming more determined than ever to improve the patient experience for others.
He and his wife now work with medical and care professionals, carers groups and the public to improve understanding of the effects of brain injury.
He said: "It was during my recovery that I became a real stroke specialist.
"I want people to know that one can work in the field of brain injury for decades and yet not fully understand what survivors are going through.
"If I could return to my work I would 'appreciate' my patients differently now.
"You need to ask the patient how it feels for them, don't just assume that you know because you read it in a book. It's not enough.”
For his decades of work to help brain injury survivors Prof Kischka has been nominated for Stephen McAleese Outstanding Contribution to Headway Award at the charity’s annual awards.
Chief executive of Headway Oxfordshire Jamie Miller, said: "His focus on improving the lives of others is genuine and tireless, despite his own daily challenges.
"His personal tragedy has only gone to strengthen his resolve to make a difference to those around him and his community.
"Udo is a delightful, kind person who strives for others and he thoroughly deserves some recognition for his extraordinary efforts and good work."
The awards will be held in London on Friday, December 7.

Gene vital for post-stroke recovery identified for the first time

Say you have this gene. What EXACT REHAB PROTOCOL is still needed to get to 100% recovery? That is the only goal, nothing less. You don't get your patients there you don't get paid. 

Gene vital for post-stroke recovery identified for the first time 

Patients with certain variants of the PATJ gene have less ability to recover after suffering a stroke
IMIM (Hospital del Mar Medical Research Institute)
Having certain specific variants of the PATJ gene predisposes to worse recovery from ischemic stroke. 7 out of 10 patients with these variants suffer severe sequelae three months after having a stroke, in other words, they are in a situation of dependence, compared to less than half of patients who do not present these variants. This is data from an international, multicentre study coordinated by researchers at the Hospital del Mar Medical Research Institute (IMIM) and doctors from the Hospital del Mar, published in the journal Circulation Research. This is the most important research carried out so far in the field of genetics and stroke prognosis, and the first published: it uses data from more than 2,000 patients and involves 12 centres from around the world. The study was carried out thanks to the help of the 2010 edition of La Marató de TV3.
Dr. Jordi Jiménez Conde, coordinator of the study and attending physician at the Hospital del Mar's Neurology Department, explained that "It is the largest study published to date on the genetics and prognosis of stroke, and the first that has found consistent results and been replicated in different countries." They analysed the degree of disability after three months of more than 2,000 patients with ischemic stroke --caused by the blockage of a cerebral artery and which represents 88% of total strokes-- by studying multiple clinical factors and genetic data. Specifically, more than 5 million genetic variants were studied for each individual. "The PATJ gene shows several variants that significantly influence recovery in patients", says Dr. Jiménez Conde. It is a gene involved in cell binding that has a strong presence in nervous tissue and which has already been associated with sleep disorders and obesity.
Genetic influence on recovery
"In this study, we identified a set of genetic variants that are relatively common in the population, and which are associated with worse recovery from stroke after three months", stresses Dr. Marina Mola-Caminal, first author of the study and a researcher in the IMIM's Neurovascular Research Group. This leads the way to studying the mechanisms used by the PATJ gene to influence this process. "In the future, these variants could be used as biomarkers for stroke sufferers, and, depending on the presence of risk alleles (alternative forms of a gene) in each individual, rehabilitation strategies could be personalised."
At the same time "we are able to indicate a region of the genome that is heavily involved in neuroplasticity and neuroregeneration processes, and perhaps if we understand the pathways, we will be able develop new treatments that use this gene as a therapeutic target and help improve patient prognosis", notes Dr. Jiménez Conde.
The study also involved Dr. Israel Fernández, co-researcher in the study and participant in its design and coordination. He is currently at the Hospital de la Santa Creu i Sant Pau Research Institute but at the time of the study was part of the Vall d'Hebron Research Institute (VHIR) and Mutua de Terrassa Neurovascular Research Laboratory. Dr. Fernández comments that "All neuroprotective drugs tested to improve post-stroke recovery have failed. For that reason, this study, utilising mass genetic strategies, may be the first step towards developing new drugs that are truly effective."

Olympic mindset helps Johnson with stroke recovery

Have doctors been honest with him and said that only 10% get to almost full recovery? And that there are no protocols or training regimens to follow?

Olympic mindset helps Johnson with stroke recovery

Michael Johnson has spoken of his initial anger after discovering he had suffered a stroke but insists an Olympic mindset will enable him to make a full recovery.
The 51-year-old Olympic sprint champion says he is "pretty much back to normal" after suffering a transient ischemic attack in September.
Johnson, once the fastest man on the planet, said he had finished a training session at home when he felt a "a strange tingling down my arm and left side".
He "decided not to take any chances" and headed straight to hospital.
"After the MRI scan, I almost fell off the table. I could not walk or move my left leg," he told the BBC.

"The numbness of my arm was intense too. I could not feel my arm and moving my fingers was problematic.
"It was a lot of emotions. Once I was told I had suffered a stroke and I could not walk things get immediately real.
"You start to think: 'What is my life going to be like going forward? What is my quality of life going to be like? Will I be able to dress myself? Will I be able to take care of myself or will my loved ones have to take care of me?'
"I had a great team of doctors and they said that is what all stroke victims ask but unfortunately there is no answer to the questions - only time will tell.

"Some people make a full recovery,(10%) some make a partial recovery and how much time that takes there is no answer. That is difficult to hear and pretty scary.
"You go from fear to anger asking, 'why did this happen to me?' The first thing doctors say is not to smoke, lose weight, work out and get fit - well that is what I was doing when this happened - and eat right.
"I was doing all the right things so I was pretty angry for half a day."
Johnson, who won 200m Olympic gold at the Atlanta Games in 1996 in 19.32 seconds, said the same distance in hospital took him 15 minutes.
He added: "Doctors said the best chance of recovery was to immediately get into physical therapy.(They lied because they have nothing to back up that statement. Notice that the doctor has nothing to do.)
"I did that two days after the stroke and I got out of bed with assistance and got behind the walker around the hospital - and ironically it was around 200m. I timed it and it took me around 15 minutes to cover that distance.
"Ordinarily that would be very disconcerting and I would have no hope - having been the fastest person in the world at that distance - but I was very encouraged.
"For the next few weeks I went back into an Olympic mindset and focusing on having the best training session I can today and using it to be better and get better. Almost three months on now from the stroke and I am pretty much back to normal and back to work."

Sunday, December 9, 2018

How is your doctor applying fixed vs. growth mindset to your stroke recovery?

Does your doctor have any clue what this even is? I'm sure mine is growth.

How is your doctor applying fixed vs. growth mindset to your stroke recovery? 

Can't copy and paste, you'll have to read at link.

Tree removal

After coming back from Portugal this 10" log needed to be cut thru and moved. My battery powered chainsaw only lasts 4 minutes at a time, so in 5 days I visited it 10 times and still had to cut the last inch by hand. I haven't tried my gas powered chainsaw yet, maybe that vibration would be enough to kickstart my left arm/wrist/hand recovery. WHOM DO I GO TO TO ASK THAT QUESTION?

5 Books Your Brain Needs to Read for Its Own Good by Debbie Hampton

My 5 highest books are a little different because they are more associated with stroke recovery: 

Stronger After Stroke by Peter Levine.

Stroke After Stroke: A Rower's Pilgrimage by Barbara Polan

Sensory Re-Education of the Hand after Stroke by Margaret Yekutiel 

A Therapist Goes Home After a Stroke by Rebecca Dutton

The woman who changed her brain : and other inspiring stories of pioneering brain transformation / Barbara Arrowsmith-Young 


5 Books Your Brain Needs to Read for Its Own Good by Debbie Hampton 

More details at link. 
Below are five books which I highly recommend for anyone with a brain….and they just also happen to be the ones from which I have written the most blogs! 

Soft-Wired: How the New Science of Brain Plasticity Can Change Your Life

Hardwiring Happiness: The New Science of Contentment, Calm, and Confidence

The Upward Spiral: Using Neuroscience to Reverse The Course of Depression, One Small Change at a Time

The Brain That Changes Itself

 Buddha’s Brain                                    

Ask your stroke doctor why they haven't gone back to blood letting since they really haven't implemented any later research?

We may as well go back to blood letting as a stroke prescription as discussed in the 1843 book, 'An Essay On The Nature and Treatment of Apoplexy'. What was the last stroke rehab protocol your hospital has implemented? Guidelines and recommendations don't count, only lazy persons claim that as useful repeatable rehab.

Evaluating stroke research and stroke articles/books - Great stroke association responsibilities

How we should have stroke information evaluated for us. Individual stroke doctors and stroke hospitals are not doing any of this.  Having 10 million stroke survivors every year do this evaluation is the height of stupidity.

  1. What in here could be used to update or create a stroke  protocol?
  2. What research should we sponsor based on this to either recover from stroke or prevent  stroke?
  3. What do we need to write on our website or put out as a press release? 
  4. What needs to be pushed out to all stroke therapists, doctors or hospitals?
  5. Every week the same questions would be asked on the research  that came out that week.

Statin Medication Enhances Progression of Coronary Artery Calcification: The Heinz Nixdorf Recall Study

I don't have enough medical brain power to understand so ask your doctor for it in understandable terms.  So you can ask whether better stroke recovery is more important than calcifying your arteries.

Simvastatin attenuates axonal injury after experimental traumatic brain injury and promotes neurite outgrowth of primary cortical neurons  Oct. 2012

Or these competing narratives;

Statins associated with improved heart structure and function May 2017 

Stroke Rounds: Statin Users Have Better Outcomes February 2016

Statins induce angiogenesis, neurogenesis, and synaptogenesis after stroke

September 2011 

New study strengthens evidence of the connection between statin use and cataracts  December 2014 

Stroke Patients Boost Survival by Getting Statins in Hospital    October 2014





Statin Medication Enhances Progression of Coronary Artery Calcification: The Heinz Nixdorf Recall Study

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Statins are suggested to stabilize plaque by decreasing lipid-rich and necrotic plaque components and increasing plaque calcification 1, 2. However, to date the relationship between statin administration and progression of coronary artery calcification (CAC) is poorly understood, and existing data are limited to patient cohorts and relatively short follow-up times. Therefore, in this study, we aimed to investigate whether the use of statins influences the progression of CAC during >5 years of follow-up in an observational study based on participants from the general population cohort of the Heinz Nixdorf Recall Study, free from clinical cardiovascular disease at baseline (3). CAC score was assessed using electron-beam computed tomography at baseline and after 5 years using an identical scanning protocol and quantified by the Agatston score. Regression analysis was used to determine the association of CAC progression with statin intake, with log transformation of CAC to normalize for its distribution.
We included 3,483 participants (mean age 59 ± 8 years, 47% men) in this analysis. Overall, 230 subjects received statin medications at baseline. Median CAC scores at baseline were 58.8 (interquartile range [IQR]: 2.6 to 273.3) for subjects with statin intake and 5.9 (IQR: 0 to 80.2) for subjects without. Median follow-up CAC scores were 141.3 (IQR: 19.6 to 554.7) for subjects with statin intake and 21.2 (IQR: 0.0 to 174.6) for those without.
In unadjusted regression analysis, taking a statin was associated with 39% higher progression in CAC+1 (Table 1). This relationship was slightly attenuated after adjustment for cardiovascular risk factors but remained statistically significant, with approximately 31% higher progression of CAC+1, attributable to statin intake. Likewise, subjects with statin intake had almost 2-fold odds for CAC progression greater than the expected range compared with subjects without statin medication in unadjusted and adjusted regression analyses.

Tables and more at link. 

“Plans are of little importance, but planning is essential.” - Winston Churchill

I see nothing anywhere in the stroke world that any planing to solve problems in stroke is occurring. All I see is lazy press releases.

Brain Bean - The Smart Roasted Coffee!

An ad I got, since there is nothing here but fluff, ask your doctor if this is accurate and what the exact diet protocol for it is.

Brain Bean - The Smart Roasted Coffee!

Small Batched, Smart Roasted Coffee that Maximizes and Keeps 5-10X the Health Promoting Chlorogenic Acid (CGA) than Traditionally Roasted Coffee

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Acupuncture MRI Results After Ischemic Stroke

Really? Impossible to have effects except as a placebo. Energy meridians have never been proven to exist.
No mechanism of action is possible.

Acupuncture MRI Results After Ischemic Stroke 

Acupuncture regulates brain regions for ischemic stroke patients. Southern Medical University researchers gathered MRI data in a controlled clinical trial consisting of both healthy subjects and patients suffering from ischemic stroke. In a controlled human clinical trial, Waiguan (TB5) applied unilaterally to the right arm produced significant MRI findings. True acupuncture caused important changes in brain functional connectivity.
The researchers determined that true acupuncture triggers significant negative activation in the default mode network (DMN) and other brain regions specific to the Traditional Chinese Medicine (TCM) indications of Waiguan. The DMN is a network of highly correlated brain regions, which is active under resting-state conditions. In addition, they found that ischemic stroke affects the brain’s overall response to acupuncture. The healthy control group and the ischemic stroke group had different negatively-activated brain regions in the DMN when receiving true acupuncture. [1]

Waiguan (TB5)
The earliest introduction of Waiguan was found in the Huangdi Neijing (The Yellow Emperor’s Classic of Medicine). Waiguan is the luo-connecting point of the hand shaoyang sanjiao meridian as well as one of the eight confluent points. It is the confluent point of the yang linking vessel. Needling Waiguan is indicated for the treatment of the following disorders: upper limb disorders (e.g., upper limb paralysis, pain, numbness, swelling and other motor and sensory dysfunction), head and sensory organ disorders (e.g., migraines, red and swollen eyes, tinnitus, deafness), fever and exogenous diseases (e.g., common cold, febrile illnesses). The researchers found that needling Waiguan raises negative activation in the somatic motor cortex, somatic sensory cortex, visual information processing cortex, and auditory information process cortex.

In the normal control group, the brain regions deactivated by real acupuncture included the left superior parietal lobule, left inferior parietal lobule, left precuneus, left superior frontal gyrus, left precentral gyrus, left postcentral gyrus, left occipital lobe, right precentral gyrus, right postcentral gyrus, right precuneus, and right cuneus. The precentral gyrus and superior frontal gyrus are involved in somatic motor functions. The superior parietal lobule and postcentral gyrus are associated with somatic sensory functions. The occipital lobe interprets visual information. The aforementioned regions are specific to the indications of Waiguan. The inferior parietal lobule, occipital lobe, and precuneus are DMN related regions. On the other hand, the brain regions deactivated by sham acupuncture included the left precentral gyrus, left postcentral gyrus, and right superior frontal gyrus. The results indicate specific brain activation patterns associated with true acupuncture and sham acupuncture respectively.
In the ischemic stroke group, the brain regions deactivated by real acupuncture included the left medial frontal gyrus, left postcentral gyrus, left middle temporal gyrus, right postcentral gyrus, right precentral gyrus, and right medial frontal gyrus. The middle temporal gyrus is associated with interpreting auditory information. It is regarded as a Waiguan indication-specific region along with the precentral gyrus, postcentral gyrus, and middle temporal gyrus. The medial frontal gyrus is a part of DMN regions. By contrast, the brain regions deactivated by sham acupuncture included the left and right precuneus.

The researchers (Zhang et al.) used the following study design. A total of 44 subjects participated in the study and were divided into two groups, with 24 and 20 subjects in each group respectively. The treatment group subjects were selected from the Nanfang Hospital and the First Affiliated Hospital of Guangzhou University of Traditional Chinese Medicine. The treatment group patients were diagnosed with ischemic stroke. The control group subjects included healthy volunteers.
The statistical breakdown for each group was as follows. The treatment group was comprised of 10 males and 10 females. The mean age of the treatment group was 52.8 years. The mean weight was 50.3 kg. The mean height was 160.3 cm. The mean course of disease was 2.2 months. The control group was comprised of 12 males and 12 females. The mean age of the control group was 24.6±3.4 years. The mean weight was 51.4 kg. The mean height was 163.4 cm. There were no significant differences in terms of their gender, age, height, and weight. Both groups were scanned using fMRIs after receiving true or sham acupuncture intervention.

Real Acupuncture
True acupuncture and sham acupuncture were performed by the same acupuncturist with clinical and research experience. Both procedures employed the use of a tube-guided device that can be attached to the skin (Park Sham Tube, AcuPrime). The Park Sham Tube needle is a research device that mimics true acupuncture; however, the needle never penetrates the skin. Instead, the needle retracts into the handle when tapped, thereby visibly appearing as true acupuncture.
After disinfection of the acupoint site, a 0.30 × 40 mm disposable filiform needle was tapped into the acupoint of each patient with a high needle entry speed, reaching a depth of 10 (±2) mm. Upon a deqi sensation, the Ping Bu Ping Xie (attenuating and tonifying) manipulation technique was applied, with a twisting range of 180 degrees and frequency of 60 times/minute. The manipulation was not employed for the first 30 seconds, it was then initiated for the second 30 seconds, and then stopped again for the third 30 second interval. The whole process was repeated continuously for a total of 180 seconds. The device was placed on the skin until the treatment session was finished.

Sham Acupuncture Treatment Simulation
The sham acupuncture group use needles with a retractable, flattened needle point. The Ping Bu Ping Xie (attenuating and tonifying) manipulation was applied. For the first 30 seconds, the needle was slightly lifted to keep the needle point away from the skin; for the second 30 seconds, the needle was tapped into the tube to make the needle point slightly touch the skin, for the third 30 seconds, the needle was lifted again. The whole process was repeated continuously for a total of 180 seconds. The device was placed on the skin until the treatment session was finished.

According to the research, true acupuncture at Waiguan regulates DMN brain regions and raises negative activation in indication-specific regions, including the somatic motor cortex, somatic sensory cortex, visual information processing cortex, and auditory information process cortex. The process was verified by repeated applications across multiple subjects and was verified by MRIs. The results indicate that acupuncture produces point-specific effects on brain regions in ischemic stroke patients.
This type of research supports additional findings by other researchers. In another investigation, Yang et al. conclude that acupuncture has the ability to “promote the proliferation and differentiation of neural stem cells in the brain… accelerate angiogenesis and inhibit apoptosis…. prevent and treat neural injuries following cerebral ischemia.” [2] Yang et al. add that GV20 (Baihui) and GV26 (Shuigou) regulate cells which “increase the release of nerve growth factors (NGFs) to make nerve cells survive and axons grow, synthesize neurotransmitters, (and) metabolize toxic substances….” In addition, the researchers note that needling CV24 (Chengjiang), CV4 (Guanyuan), GV26, and GV20 “inhibit excessive proliferation of the hippocampal astrocytes and promote cellular differentiation.”
Yang et al. also note that acupuncture at GV20 and GV14 (Dazhui) affect the contents and expression of signal transducers and activators of transcription (STATs). STATs are active in the Janus kinase STAT pathway and transmit information from chemical signals outside the cell, through the cell membrane, and into gene promoters on the DNA inside the cell nucleus (causing DNA transcription and cellular activity). Yang et al. note that acupuncture’s influence on STATs indicates that it activates self-protection and reduction of “apoptosis of the nerve cells in and around the ischemic focus.” This indicates that acupuncture has a neuroprotective effect for stroke patients.

[1] Zhang GF, Huang Y, Tang CS, Lai XS, Chen JQ. Identification of Deactivated Brain Regions by Real and Non-penetrating Sham Acupuncture Stimulation on Waiguan: An fMRI Study in Normal Versus Pathological Conditions [J]. Chinese General Practice, 2017, 20(9):1098-1103.
[2] Zhou-xin Yang, Peng-dian Chen, Hai-bo Yu, Wen-shu Luo, Yong-Gang Wu, Min Pi, Jun-hua Peng, Yong-feng Liu, Shao-yun Zhang, Yan-hua Gou. Research advances in treatment of cerebral ischemic injury by acupuncture of conception and governor vessels to promote nerve regeneration. Journal of Chinese Integrative Medicine, 01-2012. vol. 10, 1. Shenzhen Traditional Chinese Medicine Hospital, Guangzhou University of Chinese Medicine.

Saturday, December 8, 2018

Melatonin attenuates myocardial ischemia reperfusion injury via improving mitochondrial fusion/mitophagy and activating the AMPK‐OPA1 signaling pathways

Simple question. Would this work for stroke reperfusion?


It most certainly will not be our fucking failures of stroke associations.

Melatonin attenuates myocardial ischemia reperfusion injury via improving mitochondrial fusion/mitophagy and activating the AMPK‐OPA1 signaling pathways

First published: 05 December 2018
This article has been accepted for publication and undergone full peer review but has not been through the copyediting, typesetting, pagination and proofreading process, which may lead to differences between this version and the Version of Record. Please cite this article as doi: 10.1111/jpi.12542


Optic atrophy 1 (OPA1)‐related mitochondrial fusion and mitophagy are vital to sustain mitochondrial homeostasis under stress conditions. However, no study has confirmed whether OPA1‐related mitochondrial fusion/mitophagy is activated by melatonin and, consequently, attenuates cardiomyocyte death and mitochondrial stress in the setting of cardiac ischemia reperfusion (I/R) injury. Our results indicated that OPA1, mitochondrial fusion and mitophagy were significantly repressed by I/R injury, accompanied by infarction area expansion, heart dysfunction, myocardial inflammation, and cardiomyocyte oxidative stress. However, melatonin treatment maintained myocardial function and cardiomyocyte viability, and these effects were highly dependent on OPA1‐related mitochondrial fusion/mitophagy. At the molecular level, OPA1‐related mitochondrial fusion/mitophagy, which was normalized by melatonin, substantially rectified the excessive mitochondrial fission, promoted mitochondria energy metabolism, sustained mitochondrial function and blocked cardiomyocyte caspase‐9‐involved mitochondrial apoptosis. However, genetic approaches with cardiac‐specific knockout of OPA1 abolished the beneficial effects of melatonin on cardiomyocyte survival and mitochondrial homeostasis in vivo and in vitro. Furthermore, we demonstrated that melatonin affected OPA1 stabilization via the AMPK signaling pathway and that blockade of AMPK repressed OPA1 expression and compromised the cardioprotective action of melatonin. Overall, our results confirm that OPA1‐related mitochondrial fusion/mitophagy is actually modulated by melatonin in the setting of cardiac I/R injury. Moreover, manipulation of the AMPK‐OPA1‐mitochondrial fusion/mitophagy axis via melatonin may be a novel therapeutic approach to reduce cardiac I/R injury.
This article is protected by copyright. All rights reserved.

Altering the Rehabilitation Environment to Improve Stroke Survivor Activity (AREISSA): A Phase II Trial

You are attacking the problem from the wrong side. The problem is that doctors are doing ABSOLUTELY NOTHING to assist your recovery. Have them stopthe 5 causes of the neuronal cascade of death in the first week. That would assist your recovery vastly more than rehab which only fully works 10% of the time.  And just why the fuck are you studying environmental enrichment? Hasn't it been proven enough by this enriched environment talked about by Dr. Dale Corbett in 2011?

Altering the Rehabilitation Environment to Improve Stroke Survivor Activity (AREISSA): A Phase II Trial

Despite higher levels of activity being associated with better stroke recovery, stroke patients on most rehabilitation units spend the majority of their day inactive and alone.


To determine the clinical and operational feasibility and safety of Environmental Enrichment (EE)
Design: Before-after non-randomised controlled trial
Current status: Recruitment ongoing
Site/s: Bankstown Lidcombe, NSW; St Vincent’s Hospital Sacred Heart Rehabilitation Unit, NSW; Austin Health Royal Talbot, Mellor Unit, VIC, and Monash Health Kingston Centre, VIC
In animal models, Environmental Enrichment (EE) involves organisation of the environment and provision of equipment to facilitate physical, cognitive and social activity. EE promotes rewiring of the brain after stroke and has been found to significantly enhance functional recovery. Preliminary work on the use of a human model of EE using individual (eg. iPods, & word puzzles) and communal (eg. access to interactive gaming, computer, books/newspapers & jigsaws) enrichment in a rehabilitation unit indicates it encourages stroke patients to be more active. Greater activity during rehabilitation has numerous benefits, the most important of which is achieving better functional recovery and subsequently, greater independence. Altering the Rehabilitation Environment to Improve Stroke Survivor Activity (AREISSA) is a Phase II Trial involving four rehabilitation units, 2 in NSW and 2 in VIC, which seeks to determine the safety, efficacy, feasibility and patient and staff acceptability of this model of EE during stroke rehabilitation. This and the other enrichment projects conducted alongside AREISSA, will be used to inform future larger trials required to determine the effect of EE on stroke survivor recovery and quality of life.
Methods: Behavioural mapping, in-depth interview, audit and survey

Friday, December 7, 2018

A trial to Evaluate an eXTended RehAbilitation service for Stroke patients (EXTRAS)

You'll have to ask your doctor what the results were and what protocols were used to try to get more than 10% of patients 100% recovered.  It ended at the end of October so if your doctor doesn't know about this, once again incompetence reigns supreme.

A trial to Evaluate an eXTended RehAbilitation service for Stroke patients (EXTRAS)

Condition category
Circulatory System
Date applied
Date assigned
Last edited
Prospectively registered
Overall trial status
Recruitment status
No longer recruiting

Plain English Summary

Background and study aims
One third of patients have long term disability after stoke but specialist stroke rehabilitation usually lasts no more than a few months. Patients who have on going rehabilitation needs once specialist stroke rehabilitation finishes may be referred to a range of other health care professionals or services, but most do not offer specialist stroke rehabilitation. One of the reasons that specialist stroke rehabilitation is not provided over a longer period is because it is not yet known if it is beneficial. This research project is a clinical trial to determine whether a new extended stroke rehabilitation service is beneficial to patients and carers.

Who can participate?
Adults aged over 18 with a new stroke who are being discharged from hospital after their stroke under the care of an Early Supported Discharge team. Carers of stroke patients may also participate. A carer is the main family member or friend, who will provide support after discharge. He/she may not necessarily live with the patient.

What does the study involve?
Stroke patients and carers who agree to participate in the trial will be randomly allocated to either receive a new extended stroke rehabilitation service or to continue with usual NHS care when routine specialist stroke rehabilitation (Early Supported Discharge) ends. The new extended stroke rehabilitation service will involve on going contact, usually by telephone, with a senior Early Supported Discharge (ESD) stroke therapist or nurse for 18 months after ESD finishes. The therapist/nurse will contact patients and carers at 1, 3, 6, 12 and 18 months after discharge from ESD to review their progress and rehabilitation needs. Rehabilitation goals will be agreed and the therapist/nurse will give advice on how to progress towards the goals. The advice may be verbal advice, for example, exercises to practice at home. Or, if required, referral for an additional period of therapy from a service which is available locally may be arranged. Usual NHS care following specialist stroke rehabilitation may involve referral to a range of rehabilitation services in accordance with local clinical practice. The effectiveness of the new extended rehabilitation service will be evaluated by comparing the health (e.g functional abilities and quality of life) of patients and carers who received the new service with those who received usual NHS care.

What are the possible benefits and risks of participating?
We do not know if providing a specialist stroke rehabilitation service over a longer period of time is beneficial. However, we do know that rehabilitation treatments early after stroke improve health and recovery. We believe that rehabilitation over a longer period of time may be beneficial, but this is not yet proven.

Where is the study run from?
The study is being run from Newcastle University, Newcastle upon Tyne, UK. Patients and carers from twelve or more NHS stroke services will be invited to take part.

When is the study starting and how long is it expected to run for?
Recruitment to the study will start on 01 January 2013 and end on 31 May 2015. Study follow up will end on 31 January 2017. The total duration of the study is 5 years.

Who is funding the study?
UK National Institute for Health Research - Health Technology Assessment Programme.

Who is the main contact?
Dr Lisa Shaw

Trial website

Contact information



Primary contact

Dr Lisa Shaw


Contact details

Stroke Research Group
Institute for Ageing and Health
3-4 Claremont Terrace
Newcastle Upon Tyne
United Kingdom
+44 (0)191 222 6779

Additional identifiers

EudraCT number number

Protocol/serial number


Study information

Scientific title

A trial to Evaluate an eXTended RehAbilitation service for Stroke patients (EXTRAS)



Study hypothesis

To determine the clinical and cost effectiveness of an extended stroke rehabilitation service.

Ethics approval

Newcastle and North Tyneside Research Ethics Committee, 25/06/2012, ref: 12/NE/0217

Study design

Randomised interventional phase III study

Primary study design


Secondary study design

Randomised controlled trial

Trial setting


Trial type


Patient information sheet

Not available in web format, please use the contact details below to request a patient information sheet


Stroke Rehabilitation


Study intervention: An extended stroke rehabilitation service provided for 18 months following completion of routine specialist stroke rehabilitation (Early Supported Discharge). The extended stroke rehabilitation service will provide on-going contact with a senior ESD team member who will lead and coordinate further rehabilitation.

Study control: Usual care post Early Supported Discharge. Usual care may involve referral of patients to a range of rehabilitation services upon completion of ESD in accordance with local clinical practice.

Intervention type



Phase III 

Drug names

Primary outcome measure

Nottingham Extended Activities of Daily Living Scale at 24 months post randomisation.

Secondary outcome measures

For patients: health status (Oxford Handicap Scale), quality of life (Euroqol EQ-5D), mood (Hospital Anxiety and Depression Scale), experience of services and resource use (adaptation of the Client Service Receipt Inventory) at 12 and 24 months.

For carers: quality of life (Euroqol EQ-5D), carer stress (Caregiver Strain Index) and experience of services at 12 and 24 months.

Overall trial start date


Overall trial end date