Use the labels in the right column to find what you want. Or you can go thru them one by one, there are only 34,115 posts. Searching is done in the search box in upper left corner. I blog on anything to do with stroke. DO NOT DO ANYTHING SUGGESTED HERE AS I AM NOT MEDICALLY TRAINED, YOUR DOCTOR IS, LISTEN TO THEM. BUT I BET THEY DON'T KNOW HOW TO GET YOU 100% RECOVERED. I DON'T EITHER BUT HAVE PLENTY OF QUESTIONS FOR YOUR DOCTOR TO ANSWER.
Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 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:
My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. 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.
Monday, February 4, 2019
The Impact of Thrombolysis and Thrombectomy on Stroke Outcome in a Telemedicine Network
They still just talk about 'stroke care' and good clinical outcomes as if those are good measurements. The only goal to be measured in stroke is 100% recovery. Until that is the measurement, all this stroke research is a waste of time. You have one goal in stroke and you are completely failing at it. I blame the mentors and senior researchers for not stating that explicitly.
The Impact of Thrombolysis and Thrombectomy on Stroke Outcome in a Telemedicine Network
6th ESO–ESMINT–ESNR Stroke Winter School
Oh hell, what a waste, management of patients NOT interventions/protocols to get them 100% recovered. This is the exact reason everything in stroke needs to be destroyed and have survivors in charge. They are teaching status quo, which is a complete failure.
6th ESO–ESMINT–ESNR Stroke Winter School
Report of the 6th ESO ESMINT ESNR Stroke Winter School
Urs Fischer, Pasquale Mordasini, Jan Gralla, Simon Jung
Urs Fischer, Pasquale Mordasini, Jan Gralla, Simon Jung
The 6th ESO ESMINT ESNR Stroke Winter
School was held in Bern, Switzerland from the 29th January to 1st of
February 2019. The local organizing committee were Prof. Jan Gralla, PD
Dr. Pasquale Mordasini, PD Dr. Simon Jung and Prof. Urs Fischer. Joëlle
Schilling, Michela Mordasini and Helena Gerber actively supported them.
We had the difficult task to select 67
participants out of 146 applicants, but eventually 37 rising stroke
physicians and 30 neurointerventionalists arrived in Bern from the
following 22 different countries: Albania, Austria, Belgium, Croatia,
France, Germany, Greece, Israel, Italy, Latvia, Lithuania, Netherlands,
Norway, Poland, Portugal, Romania, Russia, Slovakia, Sweden,
Switzerland, Ukraine and United Kingdom.
The primary aim of the 6th ESO ESMINT
ESNR Stroke Winter School was bringing together European stroke
physicians and neurointerventionalists in order to enhance
interdisciplinary management of patients with acute ischaemic stroke.
The Stroke Winter School started on the 29th of January 2019 with the welcome of the president of the European Stroke Organization (ESO) Prof. Bart Van der Worp the representative of the president of the European Society of Minimal Invasive Neurological Therapy (ESMINT) and as well of the committee of the Interventional Neuroradiology Section of the European Society of Neuroradiology (ESNR) Prof. Jan Gralla.
The Stroke Winter School started on the 29th of January 2019 with the welcome of the president of the European Stroke Organization (ESO) Prof. Bart Van der Worp the representative of the president of the European Society of Minimal Invasive Neurological Therapy (ESMINT) and as well of the committee of the Interventional Neuroradiology Section of the European Society of Neuroradiology (ESNR) Prof. Jan Gralla.
The 32 speakers (12 from EU, 20 from
Switzerland and even one of Vietnam) including neurologists,
interventional and non-interventional neuroradiologists, neurosurgeons,
and neuropediatricians led challenging discussions. The teaching program
included 33 lectures and 4-6 tutorials. The main focus of the lectures
was interdisciplinary treatment of acute stroke. There were sessions on
acute stroke imaging, acute treatment strategies including endovascular
approaches, stroke treatment in difficult circumstances and needs to set
up an interdisciplinary stroke center. In the afternoon tutorials were
given separately for neurointerventionalists and stroke physicians.
Neurointerventionalists had the opportunity for structured hands-on
teaching in small groups on endovascular procedures with animal models
and management of complications of endovascular treatment. Stroke
physicians could learn neuroangiography on a model and they were taught
interpretations of CT and MRI by neuroradiologists.
A special highlight for the
interventional neurointerventionalists were the hands-on teaching
sessions with the animal model. Small groups of 4-5 participants were
given the opportunity to perform diagnostic angiography and endovascular
treatment procedures such as thrombectomy with multiple devices.
Another highlight was the stroke
simulation course: stroke physicians and neurointerventionalists took
part in a real-life setting with simulated clinical stroke cases:
physicians had to take care of the stroke patient and to decide on acute
stroke management. Physicians were observed by colleagues and
professionals and received feedback on their performance.
During the Stroke Winter School a faculty meeting was held with members of the ESO, ESMINT and ESNR in order to discuss future common strategies to enhance the quality of stroke management. Main topic was the training of future neurointerventionalists in areas with a current lack of experienced staff.
During the Stroke Winter School a faculty meeting was held with members of the ESO, ESMINT and ESNR in order to discuss future common strategies to enhance the quality of stroke management. Main topic was the training of future neurointerventionalists in areas with a current lack of experienced staff.
During the Stroke Winter School participants and faculty had three joint dinners to favor socialization and networking.
The following sponsors contributed to the realization of the Stroke Winter School:
Stryker, Microvention, Penumbra, Bracco, Cerenovus, Medtronic, Balt, Vascular Medical, Rapid medical, Phenox, Siemens, Boehringer Ingelheim.
Stryker, Microvention, Penumbra, Bracco, Cerenovus, Medtronic, Balt, Vascular Medical, Rapid medical, Phenox, Siemens, Boehringer Ingelheim.
The local organizing committee thanks
all the invited speakers for giving time and efforts to the Stroke
Winter School, for coming to Bern, and for delivering high quality
lectures. Their interest and passion to teach the upcoming generation of
stroke physicians and neurointerventionalists was clearly visible.
We are pleased to announce that there will be a 7th ESO ESMINT ESNR Stroke Winter School on January 28th to January 31st, 2020.
Faculty and participants of the 6th ESO ESMINT ESNR Stroke Winter School in Bern.
Sunday, February 3, 2019
First US patient in novel stem cell trial for stroke disability enrolled at UTHealth
Three problems I see with this. I see stem cell as going for a moon shot rather than tackling the solvable problems in stroke or the 5 causes of the neuronal cascade of death.
No mention of monitoring if the stem cells survived.
Using the subjective Rankin scale as a recovery measurement tool.
No mention of this as a basis of stem cells injection.
Silk Biomaterial Could Regenerate the Brain After a Stroke Dec. 2018
First US patient in novel stem cell trial for stroke disability enrolled at UTHealth
University of Texas Health Science Center at Houston
The first U.S. patient to participate in a global study of a stem
cell therapy injected directly into the brain to treat stroke disability
was enrolled in the clinical trial this week at The University of Texas
Health Science Center at Houston (UTHealth).
"At McGovern Medical School at UTHealth, we have been studying cellular therapies as a novel treatment for stroke over the past 10 years. We are very excited to partner with ReNeuron and enroll the first patient into the PISCES III study," said Sean I. Savitz, MD, the study's global principal investigator and professor and director of the Institute for Stroke and Cerebrovascular Disease at UTHealth. "This study represents an important next step in the development of novel cellular therapies for chronic stroke and, to date, is the most advanced clinical trial to determine whether neural stem cells improve recovery in patients chronically disabled by stroke."
The trial, called PISCES III, is a Phase IIb, randomized, placebo-controlled, multicenter study enrolling a total of 110 eligible ischemic stroke patients, age 35 to 75, who are experiencing persistent disability six to 12 months post-stroke. They will receive either a single dose of the ReNeuron drug called CTX0E03 DP, which is injected into the brain, or they will undergo a sham surgery. The surgeries are performed at Memorial Hermann-Texas Medical Center, a teaching hospital of McGovern Medical School.
While intravenous delivery of stem cells is being studied in clinical trials for acute stroke patients, direct delivery into the brain may have more effect for patients with chronic stroke disability, Savitz said.
"Just as in a skin wound, the brain heals in different stages," said Savitz, professer and Frank M. Yatsu, MD Chair in Neurology at McGovern Medical School. "In animal studies, direct injection in a chronic stroke setting has been shown to improve recovery and outcomes. It appears that the cells are changing the environment of the damaged area of the brain, so it is more pro-regenerative. It may be releasing factors that stimulate the repair mechanism near the area of the infarct." An infarct is a small, localized area of dead tissue resulting from failure of blood supply.
The study brings together an interdisciplinary team that includes Peng R. "Roc" Chen, MD, associate professor in the Vivian L. Smith Department of Neurosurgery; and Monica Verduzco-Gutierrez, MD, associate professor in the Department of Physical Medicine and Rehabilitation at McGovern Medical School. Chen is on the steering committee for the trial and is the surgical lead. Chen brings years of experience to the trial in the surgical administration of stem cells. Verduzco-Gutierrez is the rehabilitation lead who will oversee the assessments of mobility and cognitive function before and after the procedure.
Like Savitz, both faculty members are part of the Institute for Stroke and Cerebrovascular Disease at UTHealth, which was founded in 2017 to use the strength of UTHealth's multidisciplinary experts to advance research and clinical practice in acute stroke treatments, stroke prevention, stroke recovery, population health, and health services.
The intervention arm for PISCES III includes stereotactic surgery, which uses a three-dimensional coordinate system to precisely target the area of the brain to receive the injected therapy through a burr hole. In the placebo arm, patients will receive a tiny, partial burr hole in the skull. All patients will undergo a 12-week physical therapy program. The trial has been approved by the U.S. Food and Drug Administration.
The primary endpoint of the study is a comparison of the proportion of patients in the treated and placebo arms showing a clinically significant improvement on the Modified Rankin Scale, a measure of disability and dependence, at six months post-treatment compared with baseline. Top-line results from the study are expected in early 2020.
"At McGovern Medical School at UTHealth, we have been studying cellular therapies as a novel treatment for stroke over the past 10 years. We are very excited to partner with ReNeuron and enroll the first patient into the PISCES III study," said Sean I. Savitz, MD, the study's global principal investigator and professor and director of the Institute for Stroke and Cerebrovascular Disease at UTHealth. "This study represents an important next step in the development of novel cellular therapies for chronic stroke and, to date, is the most advanced clinical trial to determine whether neural stem cells improve recovery in patients chronically disabled by stroke."
The trial, called PISCES III, is a Phase IIb, randomized, placebo-controlled, multicenter study enrolling a total of 110 eligible ischemic stroke patients, age 35 to 75, who are experiencing persistent disability six to 12 months post-stroke. They will receive either a single dose of the ReNeuron drug called CTX0E03 DP, which is injected into the brain, or they will undergo a sham surgery. The surgeries are performed at Memorial Hermann-Texas Medical Center, a teaching hospital of McGovern Medical School.
While intravenous delivery of stem cells is being studied in clinical trials for acute stroke patients, direct delivery into the brain may have more effect for patients with chronic stroke disability, Savitz said.
"Just as in a skin wound, the brain heals in different stages," said Savitz, professer and Frank M. Yatsu, MD Chair in Neurology at McGovern Medical School. "In animal studies, direct injection in a chronic stroke setting has been shown to improve recovery and outcomes. It appears that the cells are changing the environment of the damaged area of the brain, so it is more pro-regenerative. It may be releasing factors that stimulate the repair mechanism near the area of the infarct." An infarct is a small, localized area of dead tissue resulting from failure of blood supply.
The study brings together an interdisciplinary team that includes Peng R. "Roc" Chen, MD, associate professor in the Vivian L. Smith Department of Neurosurgery; and Monica Verduzco-Gutierrez, MD, associate professor in the Department of Physical Medicine and Rehabilitation at McGovern Medical School. Chen is on the steering committee for the trial and is the surgical lead. Chen brings years of experience to the trial in the surgical administration of stem cells. Verduzco-Gutierrez is the rehabilitation lead who will oversee the assessments of mobility and cognitive function before and after the procedure.
Like Savitz, both faculty members are part of the Institute for Stroke and Cerebrovascular Disease at UTHealth, which was founded in 2017 to use the strength of UTHealth's multidisciplinary experts to advance research and clinical practice in acute stroke treatments, stroke prevention, stroke recovery, population health, and health services.
The intervention arm for PISCES III includes stereotactic surgery, which uses a three-dimensional coordinate system to precisely target the area of the brain to receive the injected therapy through a burr hole. In the placebo arm, patients will receive a tiny, partial burr hole in the skull. All patients will undergo a 12-week physical therapy program. The trial has been approved by the U.S. Food and Drug Administration.
The primary endpoint of the study is a comparison of the proportion of patients in the treated and placebo arms showing a clinically significant improvement on the Modified Rankin Scale, a measure of disability and dependence, at six months post-treatment compared with baseline. Top-line results from the study are expected in early 2020.
###
For more information on whether patients may qualify for enrollment
in the trial, call Dory Parker, research coordinator, at 713-500-7085 or
email Dorothea.M.Parker@uth.tmc.edu.
Champagne Protects the Brain From Dementia
You're likely to get dementia. What is your doctors' protocol to prevent that? 1 bottle equals 5 pours so you need a partner for this. Shouldn't be hard to find. But nothing on how expensive it needs to be. But then cheap champagne tastes shitty.
The reason you need dementia prevention:
1. A documented 33% dementia chance post-stroke from an Australian study? May 2012.
2. Then this study came out and seems to have a range from 17-66%. December 2013.
3. A 20% chance in this research. July 2013.
4. Dementia Risk Doubled in Patients Following Stroke September 2018
5. Parkinson’s Disease May Have Link to Stroke March 2017
You could do coffee like I do:
How coffee protects against Parkinson’s Aug. 2014
Coffee May Lower Your Risk of Dementia Feb. 2013
Champagne Protects the Brain From Dementia
Here’s a good reason to make a toast: Researchers
have found that a compound in grapes used to make champagne can improve
spatial memory.
“The results were dramatic,” says Jeremy Spencer, a professor at the University of Reading in England and one of the investigators on the study’s research team.
“The compounds were found to favorably alter a number of proteins linked to the effective storage of memories in the brain.”
The researchers found that drinking three glasses of champagne weekly can protect the brain from dementia and prevent memory loss by restoring crucial proteins.
Spencer explains that when people age, the concentration of these proteins in the nervous system deteriorates. However, compounds called phenolics, like those in champagne, can replenish these resources.
“The research is exciting,” Spencer says, “because it illustrates for
the first time that moderate consumption of champagne has the potential
to influence cognitive function such as memory.”
Researchers attribute the brain-boosting benefits of champagne to phenolic compounds found in Pinot Noir and Pino Meunier, the two red grape varietals used to produce the alcohol. Red wine has been shown to have similar brain-boosting benefits but those are thought to come from the flavonoids in the wine.
Spencer says, “champagne, which lacks flavonoids, is also
capable of influencing brain function through the actions of smaller
phenolic compounds, previously thought to lack biological activity.”
It’s important to note that the research was conducted in rats, not humans, so experts advise proceeding with caution because rats and humans are considerably different when it comes to brain chemistry.
It’s also important to note that researchers used the pinot noir and
pinot meunier grapes that come from the Champagne region of France.
Champagne may have more health benefits than other sparkling wines like
prosecco or domestic bubbly, according to Healthy Eating.
“The results were dramatic,” says Jeremy Spencer, a professor at the University of Reading in England and one of the investigators on the study’s research team.
The researchers found that drinking three glasses of champagne weekly can protect the brain from dementia and prevent memory loss by restoring crucial proteins.
Spencer explains that when people age, the concentration of these proteins in the nervous system deteriorates. However, compounds called phenolics, like those in champagne, can replenish these resources.
Researchers attribute the brain-boosting benefits of champagne to phenolic compounds found in Pinot Noir and Pino Meunier, the two red grape varietals used to produce the alcohol. Red wine has been shown to have similar brain-boosting benefits but those are thought to come from the flavonoids in the wine.
It’s important to note that the research was conducted in rats, not humans, so experts advise proceeding with caution because rats and humans are considerably different when it comes to brain chemistry.
© 2019 Newsmax. All rights reserved.
Read Newsmax: Champagne Protects the Brain From Dementia | Newsmax.com
Urgent: Your Heart Attack Risk Determined Online - More Info
Special Report: Research is 'transforming expectations' about treating, managing stroke
I don't know where this reporter is getting his information but I see nothing out there raising expectations about stroke recovery. Agreat stroke association president would get the record corrected and point out all the problems in stroke still needing fixing.
Special Report: Research is 'transforming expectations' about treating, managing stroke
By John Joyce – Reporter, Triad Business Journal
Updated
"We have, through research, transformed the expectations of managing stroke."
Subscribe to get the full story.
LSU students help rehabilitate stroke victims with adaptive guitar
I can't tell from this if this is compensation and just one-handed playing or actual recovery working on the affected hand.
LSU students help rehabilitate stroke victims with adaptive guitar
Stroke victims now have a creative option for their rehabilitation, thanks to a team of University students who have built an adaptive guitar specializing in restoring motor function.
The guitar, which is the second of its kind, was originally the brainchild of Assistant Professor of Kinesiology, Nikita Kuznetsov.
“I have a friend who had a stroke and he was a musician,” Kuznetsov said. “He basically couldn’t play anymore, and he had played the guitar. I thought this might be one way to help him.”
Kuznetsov said his friend tried to develop a similar device, but couldn’t get it to work. Whenever Kuznetsov started his faculty position at the University, he saw it as the perfect opportunity to continue his friend’s work.
Kuznetsov enlisted a diverse team ranging from undergraduate freshmen to alumni to work on the project. Kinesiology graduate student Marcelline Dechenaud immediately jumped on board, since it was a unique opportunity to combine her academic interest in kinesiology with her musical hobby.
“I’m a musician,” Dechenaud said. “When I heard about the project, I thought that would be a very cool thing for me to be involved in.”
Dechenaud plays the cello but finds it difficult to devote time to music amidst her academic pursuits.
“I wouldn’t do it professionally, since I don’t have enough time, but I try to practice as much as I can,” Dechenaud said.
Kinesiology freshman Sarah Cherry was excited to have been included in such a meaningful project during her first year at the University.
“This is my first experience with research at a university setting,” Cherry said. “It’s such a great opportunity for me to be involved in during my freshman year of college.”
Each year in the U.S., an estimated 795,000 people suffer from a stroke. Despite popular misconception, it is not a rare condition that only affects the elderly. It is extremely common, and can happen to anyone at anytime.Recovering from a stroke can also be a lifelong process.
“I think this is something that I think a lot of people can understand and relate to,” Cherry said. “It’s easy for me to get excited about, because it has such an awesome impact on people.”
Although the adaptive guitar has only been tested on University student volunteers, the University will soon bring the device to Baton Rouge General Hospital. Kuznetsov is currently working on a grant to expand funding for the project.
“This project involves a lot of people, so it’s a great motivator,” Kuznetsov said. “We’re all in this together.”
The project is still seeking volunteers and welcomes anyone who wants to experiment with playing their adaptive guitar. Kuznetsov compared the experience to the popular music game Guitar Hero, although the technique involved is significantly more difficult. Students should not get discouraged if they initially find playing the instrument challenging, especially since they are instructed to play with their non-dominant hand.
“Some students get very frustrated the first day,” Cherry said. “It moves very quickly, so they get overwhelmed at first.”
The adaptive guitar has the added benefit of being like a starter guitar for students who are not musical. Although it can be difficult at first, most of the test subjects got the hang of it quickly.
“After the first few days, it was so easy, they weren’t concentrating anymore, and so then that’s the reason they would mess up,” Dechenaud said.
The benefits of the adaptive guitar not only apply to stroke victims or those seeking to learn how to play an instrument on a basic level. Seasoned musicians might be fascinated by the guitar’s capability to play chords that are impossible on a standard acoustic due to the complex hand placement.
LSU alumnus James Kirsch, who graduated with his bachelor’s in engineering but still remains closely involved with the project, said the project had its fair share of doubters. The idea has been attempted multiple times before, but this version is by far the most complicated and the most successful.
“No one else expected it to work,” Kirsch said. “They thought it was too complicated. When we finally presented it, one of the guys who said there was no way it was going to work said, ‘I don’t understand how you did this.’ He called it black magic.”
Despite the skeptics, Kirsch said the team always remained confident. It took a lot of long nights, but they eventually accomplished their goals.
“A few days before, I realized it wasn’t physically possible to put it together, so I had to make a lot of last minute modifications,” Kirsch said.
Although Kirsch emphasized the stress the team was under in the last few days before the presentation, he mentioned his respect for Kuznetsov as an inspiration.
“Nikita’s great,” Kirsch said. “Making him happy was worth it.”
Although the difficult part of developing the device is over, Kuznetsov said that his project has a higher ultimate goal of becoming a commonplace rehabilitation method.
“I want to do something that helps with the quality of life in the community,” Kuznetsov said. “Down the line, this could be used for people with Parkinson’s, children with autism or aging adults. It could really be helpful in a variety of situations.”
Picture at link.
Hepatocyte Growth Factor-Preconditioned NeuralProgenitor Cells Attenuate Astrocyte Reactivity andPromote Neurite Outgrowth
Your doctor can explain to you exactly why you need neurite outgrowth and the protocols they are providing to do just that. Or will incompetence reign and nothing will be provided?
- neurite elongation (1)
- neurite outgrowth (24)
Hepatocyte Growth Factor-Preconditioned NeuralProgenitor Cells Attenuate Astrocyte Reactivity andPromote Neurite Outgrowth
Dragas, Rachel.
University of Toronto (Canada), ProQuest Dissertations Publishing, 2018. 10793181.
Only a 24 page thesis.
Home-based virtual rehabilitation for upper extremity functional recovery post-stroke
Your stroke hospital can compare it to the intersection of these research articles to see what intervention can guarantee results. That word guarantee is very important. Demand your doctor explain why they don't use it.
- upper limb
(283 posts)
- virtual reality
(105 posts)
- virtual reality games
(6 posts)
- virtual reality goggles
(1 post)
- virtual reality training
(13 posts)
Home-based virtual rehabilitation for upper extremity functional recovery post-stroke
Qiu, Qinyin, PhD; Cronce, Amanda; Fluet, Gerald, PT, DPT, PhD; Patel, Jigna, PT; Merians, Alma, PT, PhD; et al.
Journal
of Alternative Medicine Research, suppl. Special Issue: Innovations and
challenges in the use of virtual reality technologies for
rehabilitation; Hauppauge Vol. 10, Iss. 1, (2018): 27-35.
One page at link.
An adaptive fall-free rehabilitation mechanism for ischemic stroke rat patients
How can your doctor use this information to translate this to human rehab? Or will NOTHING BE DONE since everyone in stroke is
waiting for SOMEONE ELSE TO SOLVE THE PROBLEM?
An adaptive fall-free rehabilitation mechanism for ischemic stroke rat patients
Abstract
Today’s
commercial forced exercise platforms had been validated not as a
well-designed rehabilitation environment for rats with a stroke, for the
reason that rat with a stroke cannot take exercise at a constant
intensity for a long period of time. In light of this, this work
presented an adaptive, fall-free ischemic stroke rehabilitation
mechanism in an animal model, which was implemented in an
infrared-sensing adaptive feedback control running wheel (IAFCRW)
platform. Consequently, rats with a stroke can be safely rehabilitated
all the time, and particularly at full capacity for approximately one
third of a training duration, in a completely fall-free environment
according to individual physical differences by repeated use of an
acceleration/deceleration mechanism. The performance of this platform
was assessed using an animal ischemic stroke model. The IAFCRW therapy
regimen was validated to outperform a treadmill and a conventional
running wheel counterpart with respect to the reduction in the
neurobehavioral deficits caused by middle cerebral artery occlusion
(MCAo). IAFCRW is the first adaptive forced exercise training platform
short of electrical stimulation-assistance in the literature, and
ischemic stroke rats benefit more in terms of the behavioral tests run
at the end of a 3-week rehabilitation program after a stroke thereby.
Introduction
Medical
expense in ischemic stroke patents has long been considered a huge
burden to health care companies in many countries, and patients often
experience difficulty performing their activities of daily living1,2.
Therefore, an effective and completely safe rehabilitation program is
seen as crucial to improve patients’ quality of life, and increasing
evidence has suggested that physical exercise can enhance the
neurological function and motor recovery after stroke3,4,5. In addition, post-ischemic stroke exercise rehabilitation has been proposed as a practical cerebral stroke treatment6,7,8.
Rodent, e.g. rat, injury models are frequently employed as a
preliminary approach to validating the effectiveness of physical
rehabilitation methods5,9,10,
and rats are trained at a fixed running speed over a specified time
period. These rehabilitation methods have been validated as effective in
cerebral stroke prevention11,12, while has been found not to be as effective in cerebral stroke rehabilitation13,14
as in prevention. A reason behind this is that these forced platforms
are designed to train normal and healthy rats, but their training
parameters could not be directly applied to cerebral stroke
rehabilitation programs.
There exist a number of limitations on today’s training platforms, including treadmills and running wheels. Rats are stimulated when they run at the end of treadmill runways, accounting for part of a physiological outcome15. Therefore, treadmill data were very likely to be collected with an interference factor induced by electric shocks. Moreover, electric shock may impose stress on or directly hurt the rats during rehabilitation13,14. Running wheel platforms can be designed as either a voluntary or a motorized form. As its name indicates, rats are permitted to run voluntarily on a voluntary running wheel. However, due to individual differences, this type of running wheel platforms often yields large variations in the final results. To avoid such discrepancies, rats often needed to be selected carefully in advance16,17, and voluntary running wheels were not treated as a key issue. As pointed out in18, rats were afraid of running, held on to the cross bars of a wheel or even stopped running, when trained using commercially available motorized running wheels (MRWs). In addition, commercially available running wheels with a diameter of 35 cm and a width of 12 cm were generally too small for average sized white rats, and were liable to cause rat patient injury19. In addition, it is more difficult to run on a curved runway than on a flat one, and rats often accidentally fell or tumble20,21. Therefore, this study aims to develop and then integrate an adaptive training mechanism into a larger sized running wheel for an improved motor function recovery after stroke.
For the sake of an improved recovery quality, a training mechanism must be made adaptive together with a low level of interference according to the physical conditions of rats during rehabilitation. Previous studies suggested that the stress response to electrical shocks in treadmills resulted in adverse physiological injuries, such as adrenal hypertrophy, splenic atrophy and circulating corticosterone22,23,24. For those taking a rehabilitation program, stress response could be a destructive factor to their recovery13, and is as well an uncontrolled parameter that can affect the final neurological outcomes. Therefore, it is advantageous to remove such potential disadvantages for the sake of clinical research. This study reviewed a number of running wheel platforms that were developed to assist in the effective recovery of rats with an ischemic stroke but short of electric shock. Utilizing an IR sensor-embedded wheel module to detect the running position of a rat, an acceleration/deceleration mechanism was enabled herein in such a way that rats were rehabilitated well in a completely fall-free environment, and adaptively within their capacity for an improved motor function recovery and a reduced cerebral infarct volume.
There exist a number of limitations on today’s training platforms, including treadmills and running wheels. Rats are stimulated when they run at the end of treadmill runways, accounting for part of a physiological outcome15. Therefore, treadmill data were very likely to be collected with an interference factor induced by electric shocks. Moreover, electric shock may impose stress on or directly hurt the rats during rehabilitation13,14. Running wheel platforms can be designed as either a voluntary or a motorized form. As its name indicates, rats are permitted to run voluntarily on a voluntary running wheel. However, due to individual differences, this type of running wheel platforms often yields large variations in the final results. To avoid such discrepancies, rats often needed to be selected carefully in advance16,17, and voluntary running wheels were not treated as a key issue. As pointed out in18, rats were afraid of running, held on to the cross bars of a wheel or even stopped running, when trained using commercially available motorized running wheels (MRWs). In addition, commercially available running wheels with a diameter of 35 cm and a width of 12 cm were generally too small for average sized white rats, and were liable to cause rat patient injury19. In addition, it is more difficult to run on a curved runway than on a flat one, and rats often accidentally fell or tumble20,21. Therefore, this study aims to develop and then integrate an adaptive training mechanism into a larger sized running wheel for an improved motor function recovery after stroke.
For the sake of an improved recovery quality, a training mechanism must be made adaptive together with a low level of interference according to the physical conditions of rats during rehabilitation. Previous studies suggested that the stress response to electrical shocks in treadmills resulted in adverse physiological injuries, such as adrenal hypertrophy, splenic atrophy and circulating corticosterone22,23,24. For those taking a rehabilitation program, stress response could be a destructive factor to their recovery13, and is as well an uncontrolled parameter that can affect the final neurological outcomes. Therefore, it is advantageous to remove such potential disadvantages for the sake of clinical research. This study reviewed a number of running wheel platforms that were developed to assist in the effective recovery of rats with an ischemic stroke but short of electric shock. Utilizing an IR sensor-embedded wheel module to detect the running position of a rat, an acceleration/deceleration mechanism was enabled herein in such a way that rats were rehabilitated well in a completely fall-free environment, and adaptively within their capacity for an improved motor function recovery and a reduced cerebral infarct volume.
High intensity physical rehabilitation later than 24 hours post stroke is beneficial in patients: A Pilot Randomized Controlled Trial (RCT) Study in mild to moderate ischemic Stroke
Andrew Marr of the UK however blames high-intensity exercise for his stroke.
If you can do high intensity training that soon you had a small stroke.
You might want to consult your doctor on this. Bet s/he doesn't even know about Andrew Marr.
High intensity physical rehabilitation later than 24 hours post stroke is beneficial in patients: A Pilot Randomized Controlled Trial (RCT) Study in mild to moderate ischemic Stroke
- 1Beijing Luhe Hospital, Capital Medical University, China
- 2Wayne State University School of Medicine, United States
Materials and Methods: We conducted a randomized and controlled trial with a blinded follow-up assessment. Patients with ischemic stroke, first or recurrent, admitted to stroke unit within 24 hours after stroke onset were recruited. Eligible subjects were randomly assigned (1:1:1) to 3 groups: Early Routine Mobilization in which patients received <1.5 h/d out-of-bed mobilization within 24-48 h after stroke onset, Early Intensive Mobilization in which patients initiated ≥3h/d mobilization at 24-48 h after the stroke onset, and Very Early Intensive Mobilization in which patients received≥3h/d mobilization within 24 h. The modified Rankin Scale score of 0-2 was used as the primary favorable outcome.
Results: We analyzed 248 of the 300 patients (80 in Early Routine Mobilization, 82 in Very Early Intensive Mobilization and 86 in Early Intensive Mobilization), with 52 dropping out (20 in Early Routine Mobilization, 18 in Very Early Intensive Mobilization and 14 in Early Intensive Mobilization). Among the three groups, the Early Intensive Mobilization group had the most favorable outcomes at 3-month follow-up, followed by patients in the Early Routine Mobilization group. Patients in Very Early Intensive Mobilization received the least odds of favorable outcomes. At 3 month follow up, 53.5%, (n=46 ) of patients with Early Intensive Mobilization showed a favorable outcome (modified Rankin Scale 0-2)(p=0.041) as compared to 37.8% (n=31) of patients in the Very Early Intensive Mobilization.
Conclusions: Post-stroke rehabilitation with high intensity physical exercise at 48 h may be beneficial. Very Early Intensive Mobilization did not lead to a favorable outcome at 3 months. Trial registration: ChiCTR-ICR-15005992.
Keywords:
Acute care, ischemic stroke, early mobilization., Intensity, Rehabilitation
* Correspondence: Prof. Yuchuan Ding, Wayne State University School of Medicine, Detroit, United States, yding@med.wayne.edu
Received: 29 Nov 2018;
Accepted: 28 Jan 2019.
Edited by:
Nicola Smania, University of Verona, Italy
Nicola Smania, University of Verona, Italy
Reviewed by:
Alessandro Picelli, University of Verona, Italy
Paolo Tonin, Sant'Anna Institute, Italy
Copyright: © 2019 Tong, Cheng, Rajah, Duan, Cai,
Zhang, Du, Geng and Ding. This is an open-access article distributed
under the terms of the Creative Commons Attribution License (CC BY).
The use, distribution or reproduction in other forums is permitted,
provided the original author(s) and the copyright owner(s) are credited
and that the original publication in this journal is cited, in
accordance with accepted academic practice. No use, distribution or
reproduction is permitted which does not comply with these terms.
Alessandro Picelli, University of Verona, Italy
Paolo Tonin, Sant'Anna Institute, Italy
* Correspondence: Prof. Yuchuan Ding, Wayne State University School of Medicine, Detroit, United States, yding@med.wayne.edu
Rehabilitation after stroke: evidence, practice, and new directions
I'm sure that there is absolutely nothing new in here. I've been following stroke research now for 8 years and shit like this is just rehashing guidelines. NOT PROTOCOLS. Until we get to protocols stroke survivors will continue to be screwed. And yes, Julie Bernhardt is a very famous stroke researcher in Australia. I take no prisoners in my pursuit of 100% stroke recovery.
Rehabilitation after stroke: evidence, practice, and new directions
First published: 28 January 2019
Summary
The process of rehabilitation involves harnessing and
optimizing the recovery processes, to enable people with stroke to lead
active, independent lives with the best possible quality of life. Stroke
recovery is an ongoing process that may continue for months or years.
This chapter draws on the most recent international Clinical Guidelines
for stroke rehabilitation to present an overview of the current evidence
for effective rehabilitation interventions. We highlight a few key
areas, focusing on physical rehabilitation, and present aspirational
vision for the future of recovery and rehabilitation after stroke.
Impact of Diet and the Gut Microbiome on Neurodegeneration and Regeneration in Neurological Disorders
Hope your doctor can read German and can use this to set up a protocol to help your recovery. Maybe even a diet protocol.
Impact of Diet and the Gut Microbiome on Neurodegeneration and Regeneration in Neurological Disorders
Barbara Gisevius MD / Aiden Haghikia MD / Sarah Hirschberg MD
Published Online: 2019-01-30 | DOI: https://doi.org/10.1515/nf-2018-0013
30,00 € / $42.00 / £23.00
Get Access to Full TextZusammenfassung
Aktuelle Forschungsergebnisse im Bereich neurodegenerativer Erkrankungen deuten vermehrt darauf hin, dass die Ernährung und damit assoziiert die Zusammensetzung des Darm-Mikrobioms einen entscheidenden Einfluss auf die Entstehung und den Verlauf verschiedenster Krankheiten haben. Die sogenannte Darm-Hirn Achse, oder präziser die Darm-Mikrobiom-Hirn Achse hat dadurch deutlich an Aufmerksamkeit gewonnen. Dabei kann der Darm das zentrale Nervensystem auf unterschiedliche Weisen beeinflussen, I) direkt durch bakterielle Bestandteile und Metaboliten von Bakterien, II) durch Manipulation der im Körper zirkulierenden Immunzellen, oder III) durch direkten Kontakt, z. B. über den N. vagus.Fortschritte auf dem Gebiet der Molekularbiologie, wie das Next Generation Sequencing ermöglichen aufgrund ihres hohen Auflösungsvermögens die genaue Identifikation von Bakterien und die Kompositionen ganzer Mikrobiome. Dadurch ist es möglich, die Interaktionen zwischen dem intestinalen Mikrobiom, dem Metabolom und dem Darm- assoziierten Immunsystem detailliert zu erforschen.
In dieser Arbeit diskutieren wir den Einfluss des Mikrobioms, der Ernährung und den damit verbundenen Gesundheitszustand auf die Neuroregeneration. Der Fokus liegt dabei auf der Möglichkeit, wie dieses Wissen in Zukunft für therapeutische Zwecke genutzt werden kann.
Abstract
Recent advances in the field of neurodegenerative disorders point to a possible association between diet, gut microbiota composition and disease incidence. Hence, the so-called gut-brain axis, or more precisely the gut-microbiome-brain axis, has gained increasing attention. There are several ways in which gut content can impact the central nervous system, i. e. either I) directly via bacterial components and dietary metabolites that are systematically available, II) by intermediates, such as circulating immune cells or III) via direct neuronal connections, i. e. the vagus nerve.New technologies for the identification of bacteria, like next generation sequencing, are enabling a higher resolution understanding of microbiota composition. Therefore, it is now possible to elucidate direct interactions between the gut microbiome, the metabolome, and the gut-associated immune system. In addition to these interactions and of equal importance are the interdependencies of gut metabolites with cells of the central nervous system. In this review, we discuss how the gut microbiome can promote neuronal regeneration or degeneration, depending on health status and diet, and how its modulation may be exploited for novel therapeutic applications.
Remyelination promoting therapies in multiple sclerosis animal models: a systematic review and meta-analysis
Do we need this after a stroke? Have we demyelinated neurons in the brain? What does your doctor know about this and what is the protocol to fix it? Scream at your doctor if you have to get her attention about actually fixing you up to 100% recovery.
Remyelination promoting therapies in multiple sclerosis animal models: a systematic review and meta-analysis
- Carlijn R. Hooijmans,
- Martin Hlavica,
- Florian A. F. Schuler,
- Nicolas Good,
- Andrin Good,
- Lisa Baumgartner,
- Gianluca Galeno,
- Marc P. Schneider,
- Tarzis Jung,
- Rob de Vries &
- Benjamin V. Ineichen
Abstract
An
unmet but urgent medical need is the development of myelin repair
promoting therapies for Multiple Sclerosis (MS). Many such therapies
have been pre-clinically tested using different models of toxic
demyelination such as cuprizone, ethidium bromide, or lysolecithin and
some of the therapies already entered clinical trials. However, keeping
track on all these possible new therapies and their efficacy has become
difficult with the increasing number of studies. In this study, we aimed
at summarizing the current evidence on such therapies through a
systematic review and at providing an estimate of the effects of tested
interventions by a meta-analysis. We show that 88 different therapies
have been pre-clinically tested for remyelination. 25 of them (28%)
entered clinical trials. Our meta-analysis also identifies 16 promising
therapies which did not enter a clinical trial for MS so far, among them
Pigment epithelium-derived factor, Plateled derived growth factor, and
Tocopherol derivate TFA-12.We also show that failure in bench to bedside
translation from certain therapies may in part be attributable to poor
study quality. By addressing these problems, clinical translation might
be smoother and possibly animal numbers could be reduced.
Introduction
Multiple Sclerosis (MS) is a chronic demyelinating disease1. With the only exception of Ocrelizumab2,
which has a modest impact on disease progression, none of the 16 FDA
approved MS therapies are able to stop or at least to decelerate the
progressively increasing disability of affected patients3.
One well-acknowledged approach to prevent disease progression is via a
boost of myelin repair. Remyelination not only restores efficient
electric conduction along axons but, because the myelin sheaths have
trophic functions for the axons4, also reduces neurodegeneration, which closely correlates with clinical disability5.
The intense search for strategies to enhance myelin regeneration to hinder further neurodegeneration and to increase clinical function of patients, is as well reflected by the large number of pre-clinical studies assessing potential remyelinating strategies. Commonly used experimental systems to study potential remyelinating therapies include neuro-inflammatory animal models such as experimental autoimmune encephalomyelitis (EAE)6 or virus-induced demyelination/inflammation7 as well as toxin-induced demyelination models with cuprizone8, lysolecithin, ethidium bromide, and complement/anti-galactocerebroside antibodies9 being the most commonly used agents of the latter group10. All of these models have strengths and limitations; whereas neuro-inflammatory models reproduce well the disseminated and inflammatory features of MS, toxin-induced demyelination models are more suited to dissect specific mechanisms of myelin decline and regeneration with a clear temporal separation of these processes and without concomitant inflammation10,11.
Cuprizone is a systemic copper-chelating agent. Upon feeding, it leads to demyelination of distinct brain regions, among them the corpus callosum. Cuprizone has a highly reproducible timeline of de- and remyelination and enables long-term demyelination when fed for a prolonged time window. The exact mechanism of cuprizone-induced demyelination is unknown10,12. Compared to Cuprizone, lysolecithin has the disadvantage of needing an invasive injection to a pre-defined CNS-position. Nevertheless, it is also highly predictive under temporal aspects. Moreover, any CNS area can be targeted selectively with this detergent13. Ethidium bromide leads to much larger areas of demyelination and degrades all nucleated cells within the injection area (including astrocytes and microglia cells)9. The local injection of Anti-galactocerebroside antibodies/complement is rarely used as toxic demyelination model. The time to complete remyelination is shorter in this model but involves a greater demyelinating area than lysolecithin10.
Many putative therapies have been identified using these toxic demyelination models, from which some already entered clinical trials. We aimed at summarizing all the already pre-clinically tested putative remyelinating therapies via a systematic review and meta-analysis in order to assess which remyelinating therapies can be promising and could be tested in clinical trials. We also investigate the efficacy of the therapies in these experimental animal models that have already entered clinical trials. We focused our analysis on the four in vivo toxic demyelination models cuprizone, lysolecithin, ethidium bromide, and complement/anti-galactocerebroside antibodies. These models might be more suited to assess potential therapies aiming at halting disease progression of progressive MS in contrast to neuro-inflammatory models, in which potential immune-modulatory effects of therapies could confound efficacy11. The results of our review should provide a framework for future clinical trials investigating putative remyelinating interventions for MS, in particular during the chronic phase of the disease when remyelination failure determines disability progression.
The intense search for strategies to enhance myelin regeneration to hinder further neurodegeneration and to increase clinical function of patients, is as well reflected by the large number of pre-clinical studies assessing potential remyelinating strategies. Commonly used experimental systems to study potential remyelinating therapies include neuro-inflammatory animal models such as experimental autoimmune encephalomyelitis (EAE)6 or virus-induced demyelination/inflammation7 as well as toxin-induced demyelination models with cuprizone8, lysolecithin, ethidium bromide, and complement/anti-galactocerebroside antibodies9 being the most commonly used agents of the latter group10. All of these models have strengths and limitations; whereas neuro-inflammatory models reproduce well the disseminated and inflammatory features of MS, toxin-induced demyelination models are more suited to dissect specific mechanisms of myelin decline and regeneration with a clear temporal separation of these processes and without concomitant inflammation10,11.
Cuprizone is a systemic copper-chelating agent. Upon feeding, it leads to demyelination of distinct brain regions, among them the corpus callosum. Cuprizone has a highly reproducible timeline of de- and remyelination and enables long-term demyelination when fed for a prolonged time window. The exact mechanism of cuprizone-induced demyelination is unknown10,12. Compared to Cuprizone, lysolecithin has the disadvantage of needing an invasive injection to a pre-defined CNS-position. Nevertheless, it is also highly predictive under temporal aspects. Moreover, any CNS area can be targeted selectively with this detergent13. Ethidium bromide leads to much larger areas of demyelination and degrades all nucleated cells within the injection area (including astrocytes and microglia cells)9. The local injection of Anti-galactocerebroside antibodies/complement is rarely used as toxic demyelination model. The time to complete remyelination is shorter in this model but involves a greater demyelinating area than lysolecithin10.
Many putative therapies have been identified using these toxic demyelination models, from which some already entered clinical trials. We aimed at summarizing all the already pre-clinically tested putative remyelinating therapies via a systematic review and meta-analysis in order to assess which remyelinating therapies can be promising and could be tested in clinical trials. We also investigate the efficacy of the therapies in these experimental animal models that have already entered clinical trials. We focused our analysis on the four in vivo toxic demyelination models cuprizone, lysolecithin, ethidium bromide, and complement/anti-galactocerebroside antibodies. These models might be more suited to assess potential therapies aiming at halting disease progression of progressive MS in contrast to neuro-inflammatory models, in which potential immune-modulatory effects of therapies could confound efficacy11. The results of our review should provide a framework for future clinical trials investigating putative remyelinating interventions for MS, in particular during the chronic phase of the disease when remyelination failure determines disability progression.
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