Use the labels in the right column to find what you want. Or you can go thru them one by one, there are only 33,819 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 neuronsthatDIEeach day because there areNOeffective 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.
Maybe, just maybe you want your doctor to analyze this to create protocols for neurogenesis AND migration of those new neurons to the needed areas. At least if they are competent they can do this. Since we have fucking failures of stroke associationseach stroke doctor in the world has to do this individually. Hope your doctor is good at creating protocols from research. There is no way to tell if this is being done properly so good luck.
Investigators have confirmed that neurogenesis occurs in discrete areas of the adult brain.
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This occurs primarily in the subventricular zone of the lateral ventricles and the subgranular zone of the dentate gyrus.
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Growth factors, neurotrophins, cytokines and hormones are the major regulators of adult neurogenesis.
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Much progress was made over the past decade on adult neurogenesis.
Abstract
The
concept of neurogenesis in the adult human brain was conceived in the
1960s, revisited in the 1980s and confirmed in the 1990s. It was a
controversial area of research due to methodological challenges. It is
now widely accepted that new neurons are continually generated in
specific regions in the adult brain. This occurs primarily in the
subventricular zone of the lateral ventricles and the subgranular zone
of the dentate gyrus in the hippocampus. Neuroblasts from the
subventricular zone migrate along the rostral migratory stream into the
olfactory bulb, whereas neuroblasts from the subgranular zone show
relatively little migratory behavior, and differentiate into dentate
gyrus granule cells. Growth factors, neurotrophins, cytokines, and
hormones are also major regulators of adult neurogenesis.
Much
progress was made over the past decade, but many questions were remain
unanswered, new insights are emerging at a stunning rate and made the
investigation of neurogenesis in the adult human brain an intense area
of research. In this review, I tried to present recent research findings
regarding basic concept, historical background, primary site, factors
influencing, clinical implications and functions of adult neurogenesis.
Literatures searched for this paper were carried out by accessing
PubMed, Google scholar, Web of science and other databases.
Do you really think your hospital is going to buy this expensive equipment? Your doctor needs to have stroke protocols that deliver trunk strengthening without this high tech piece of equipment. At least if your doctor is competent.
Rakesh Pilkar, Ph.D., will conduct a
pilot study of the AllCore360º device for improving core strength,
posture and balance in individuals with hemiplegia following chronic
stroke
Kessler Foundation
IMAGE: Dr. Pilkar monitors a demo of the
ALLCore360, the electromechanical device being tested for stroke
rehabilitation at Kessler Foundation.
view more
Credit: Kessler Foundation/Carolann Murphy
East Hanover, NJ. February 26, 2020. Researchers at Kessler
Foundation are studying a potential application of a trunk-strengthening
program to improve posture, balance, and mobility in individuals
recovering from stroke. They will test the feasibility of using an
electromechanical device called the AllCore360º Core Therapy and
Training System in the rehabilitation of stroke survivors with
hemiplegia. Rakesh Pilkar, PhD, research scientist in the Center for
Mobility and Rehabilitation Engineering Research, is the principal
investigator for the study, titled, "A novel trunk-strengthening program
for improving posture and balance for individuals with hemiplegia post
stroke," which is supported by AllCore360º (Alpharetta, GA) and Kessler
Foundation.
The impact of weakness of trunk muscles after stroke is substantial.
Adverse effects on posture and balance impair the performance of
activities of daily living, impede recovery, and limit independence.
Poor trunk control is associated with longer hospital stays, increased
risk for falls, and poorer function at discharge. "Despite evidence for
the importance of trunk control to functional outcomes in this
population, there is a lack of a standardized approach to trunk
strengthening in stroke rehabilitation," said Dr. Pilkar, "and little
information on the application of electromechanical devices for this
type of therapy.(Don't allow this lack be the excuse your doctor uses for doing nothing on protocols for this.) This pilot study enables us to test a
trunk-strengthening protocol using the AllCore360º in individuals with
hemiplegia, examine the underlying neuromuscular mechanisms, and measure
the effects on posture, balance, and walking ability," he explained.
"If preliminary findings are promising, further studies of this protocol
may be warranted."
The AllCore360º is an adjustable system that leverages gravity to
engage all trunk muscles in a 10-minute session. While seated in the
AllCore360º, the person uses isometric contraction of their trunk
muscles to hold their position while the device rotates clockwise, then
counterclockwise, at different angles and positions.
Participants will be recruited from the stroke rehabilitation
program at Kessler Institute for Rehabilitation. All participants (10 in
stroke group and 10 controls) will undergo baseline and follow-up
assessments of trunk function, balance, posture, and ambulation. The
stroke group will undergo the 4-week trunk-strengthening program,
including neuromuscular assessment using electromyography.
"We are pleased to partner with the Kessler Foundation on this pilot
study aimed at expanding options for stroke rehabilitation," said Scott
Bertrand, DC, founder and inventor of AllCore360º. "Having witnessed
the benefits of core strengthening in people seeking to improve their
health and fitness, we are optimistic that the Kessler team will see
improved outcomes in individuals recovering from stroke."
###
About AllCore360º
The Patented AllCore360° Rehabilitation Core Training System
allows patients, seniors, athletes and everyday people, to balance and
strengthen the more than 50 muscles that comprise the core in an
innovative efficient way. In multiple facilities throughout the United
States, therapists and leading edge trainers utilize the System to
promote faster recovery, improve fitness, and enhance physical
performance. The AllCore360° harnesses the forces of gravity to
challenge all of the body's core muscles in a no impact, coordinated,
isometric fashion designed to improve athletic or daily performance
regardless of ability. For more information, please visit http://www.AllCore360.com.
I have seen absolutely nothing that even remotely suggests that there is ANY objective determination of stroke damage. Without that we will never be able to competently assign stroke protocols to fix such damage. All your stroke medical 'professionals' are 'flailing in the dark' right now. But yet you are paying them for what?
Archives of Physical Medicine and Rehabilitation — Roberts PS, et al. | January 30, 2020
Researchers sought to perform a scoping
review of mild stroke definitions based on stroke severity evaluations
and/or clinical signs and symptoms reported in the literature. They
searched PubMed, PsycINFO (Ovid), and CINAHL (EBSCO) databases added
keyword combinations of a mild stroke, minor stroke, mini-stroke, mild
cerebrovascular, minor cerebrovascular, transient ischemic attack, or
TIA. For the final review, 62 studies were selected. Between January
2003 and February 2018, inclusion criteria were limited to articles
published. It was noted that inequalities in the classification of mild
stroke are evident with varying use of stroke severity assessments,
measurement cut-off scores, imaging tools, and clinical or functional
outcomes. Moreover, continued work is needed to establish a consensus
definition of mild stroke(all strokes!), which directly influences treatment receipt,
referral for services, and health service delivery.
For discussion with your doctor. Do you really think your doctor and stroke hospital keep up-to-date on stroke related research? Hell, I probably get at least twenty pieces of stroke research daily and I only can read the abstracts. So your hospital should have a dedicated employee whose only job is to summarize and distribute such research to all therapists and doctors with clear instructions on how to apply such research to get survivors 100% recovered. THAT IS WHAT A COMPETENT STROKE HOSPITAL WOULD BE DOING. Ask your stroke president if they are competent and doing such research implementation. And if not, WHY NOT?
Their reasons for doing nothing?
Laziness? Incompetence? Or just don't care? No leadership? No strategy? Not my job?
I take no prisoners in my focus on survivors, shouldn't your hospital do the same?
New
data from the ODYSSEY Outcomes trial show that alirocumab is effective
at reducing risk for any stroke without increasing risk for hemorrhagic
stroke.
In a cohort of 18,924 patients with recent ACS and elevated LDL
despite intensive statin therapy, alirocumab (Praluent,
Sanofi/Regeneron) was effective in reducing the risk for any stroke (HR =
0.72; 95% CI, 0.57-0.91) and ischemic stroke (HR = 0.73; 95% CI,
0.57-0.93), compared with placebo, during a follow-up of 2.8 years.
According to the study, these effects were achieved without increasing
the patients’ risk for hemorrhagic stroke (HR = 0.83; 95% CI,
0.42-1.65).
Moreover, researchers noted that the effect of alirocumab on stroke appeared greater for patients with higher baseline LDL but found no formal evidence of heterogeneity (P for interaction = .31).
“This analysis of the ODYSSEY Outcomes trial shows that in patients
with recent ACS and dyslipidemia despite intensive statin therapy, the
PCSK9 inhibitor alirocumab decreased the risk of stroke, irrespective of
baseline LDL and of history of cerebrovascular disease, over a median
follow-up of 2.8 years,” J. Wouter Jukema, MD, PhD,
professor of cardiology in the department of cardiology at Leiden
University Medical Center in the Netherlands, and colleagues wrote.
“Furthermore, the present findings indicate that the risk of hemorrhagic
stroke did not depend on achieved LDL levels in the alirocumab group.”
In other findings, the effect of alirocumab on stroke was similar
among individuals with previous cerebrovascular disease and those
without (P for interaction = .37). Alirocumab effect on baseline LDL
In addition, researchers found no adverse relationship between lower achieved LDL and incidence of hemorrhagic stroke in the alirocumab group compared with placebo.
“The treatment effect appeared numerically greater with lower HRs for
patients with higher baseline LDL, suggesting that patients with a
higher risk at baseline have a larger benefit of alirocumab,” the
researchers wrote. “However, this linear trend was not statistically
significant.”
In this double-blind trial, researchers randomly assigned patients
with ACS and elevated LDL to alirocumab or placebo, with target LDL
levels of 25 mg/dL to 50 mg/dL, avoiding sustained levels below 15
mg/dL. Patients were randomly assigned to alirocumab or placebo 1 to 12
months after ACS. The aim of this analysis was to evaluate nonfatal,
fatal ischemic or hemorrhagic stroke and stratified by baseline LDL
level and prior cerebrovascular disease. As Healio previously reported,
in the main results of ODYSSEY Outcomes, alirocumab reduced risk for
major adverse CV events by 15% compared with placebo in this population.
Massive gobbledegook, so no idea what this is trying to say. I know that when I practised walking movements in the pool I had much better movement and the resistance forced the spasticity to lessen.
A question SPECIFICALLY for your doctor to answer. Doesn't know, then the competent thing to do is get research going to find the answer. DOING NOTHING IS NOT OK.
In
patients with multiple intracranial aneurysms, aspirin may
significantly decrease the rate of aneurysm growth over time, according
to a study published in the Journal of Neurosurgery.
While
aneurysms >7 mm are more likely to rupture, some small aneurysms
grow, increasing the risk that they may rupture. Therefore, physicians
observe small, unruptured aneurysms over time by asking patients to
undergo regularly scheduled imaging examinations.
While there has
been some evidence that aspirin may reduce the risk of aneurysm rupture
due to the drug’s anti-inflammatory effect on the weakened aneurysm
wall, “to date, there is no medical treatment to arrest aneurysm growth
and subsequent progression to rupture,” the authors wrote.
For
the current study, Mario Zanaty, MD, University of Iowa Hospitals and
Clinics, Iowa City, Iowa, and colleagues identified 146 patients
harbouring multiple intracranial aneurysms, ≤5 mm in diameter, which had
been observed for at least 5 years. The researchers also gathered
information on the patients’ demographics, earlier medical history, the
rupture status of designated primary aneurysms, aneurysms’ angiographic
features, and treatment modalities.
In the cohort of patients,
the researchers identified a total of 375 intracranial aneurysms. At the
initial encounter, 146 aneurysms were treated and the remaining 229
aneurysms (2 to 5 mm) were observed.
During the follow-up period,
10.48% of the aneurysms grew. All aneurysms observed to grow later
underwent treatment. None of the observed aneurysms ruptured.
Multivariate
analysis showed that aspirin was significantly associated with a
decreased rate of growth (odds ratio [OR] = 0.19; 95% confidence
interval [CI], 0.05-0.63).
Variables associated with an increased
rate of growth included hypertension (OR =14.38; 95% CI, 3.83-53.94),
drug abuse (OR = 11.26; 95% CI, 1.21-104.65), history of polycystic
kidney disease (OR = 9.48; 95% CI, 1.51-59.35), and subarachnoid
haemorrhage at presentation (OR = 5.91; 95% CI, 1.83-19.09).
On
the basis of the statistical analyses, use of aspirin appears to exert a
protective effect against aneurysm growth and very likely against
future rupture.
The authors point out that their findings are observational and that future interventional studies should be conducted.
“This
study is very promising, as it outlines for the first time the
potential therapeutic effect of aspirin in decreasing aneurysm growth,”
concluded David Hasan, MD, University of Iowa Hospitals and Clinics. “If
proven in a larger study, this could offer the first cheap, effective,
over-the-counter therapeutic agent that could halt aneurysm growth and
prevent rupture.”
Cite this article: Prieto, P., Auat, F., Escobar, M., Vallejos, R., Maldonado, P., Larrain, C., Serey, M. (2019) ‘Robotic Care: A Low Cost Design to Assist Therapy for Brain Stroke Rehabilitation’, in Proceedings of the 22nd International Conference on Engineering Design (ICED19), Delft, The Netherlands, 5-8 August 2019. DOI:10.1017/dsi.2019.103 ICED19INTERNATIONAL CONFERENCE ON ENGINEERING DESIGN, ICED19 5-8AUGUST 2019, DELFT, THE NETHERLANDS ICED19 1 Prieto, Pablo (1); Auat, Fernando (2); Escobar, Maria (2); Vallejos, Ronny (3); Maldonado, Paula (4); Larrain, Cristobal (4); Serey, Martin (1) 1: Universidad Técnica Federico Santa María. Engineering Design Department.; 2: Universidad Técnica Federico Santa María. Department of Electronic; 3: Universidad Técnica Federico Santa María. Department of Mathematics; 4: Peñablanca Hospital.
ABSTRACT
A low cost robotic-assisted prototype for finger and hand rehabilitation of people affected by a stroke is presented. The system was developed by a team of undergraduate students led by a Design lecturer in collaboration with the Rehabilitation Unit of the Peñablanca Public Hospital in Chile. The system consists of a flexion sensor equipped glove, a hand exoskeleton and an Arduino control unit. The patient wears the glove in his healthy hand. When s/he performs movements with the healthy hand, the sensors register the flexion of the fingers and send this information to the servo motors installed in an exoskeleton attached to the affected hand. In this way, the affected hand reproduces the movement of the healthy hand. The system uses a combination of the mirror therapy (the patient sees his/her affected hand moving in the same way that the healthy hand does) and passive exercising (as the exoskeleton produces the movement of the hand affected by the stroke). The combination of two types of therapy in a single low cost system makes the present work unique. In the near future, the developed prototype will be used to validate the effectiveness of the new proposed robotic therapy. Keywords: Open source design, Design for health, Social responsibility, Biomedical design Contact: Prieto, Pablo Universidad Técnica Federico Santa María Engineering Design Department Chile pablo.prieto@usm.cl
So your doctors, stroke hospital and stroke association should
followup with
human research testing this out. That is the minimum a competent doctor,
stroke hospital and stroke association should be doing. But you
already know that nothing will be done unless you do this testing
yourself.
Previously
study has proved the non-erythropoietic mutant erythropoietin (MEPO)
exerted neuroprotective effects against ischemic cerebral injury, with
an efficacy similar to that of wild-type EPO. This study investigates
its effects on neurogenesis, angiogenesis, and gliogenesis in cerebral
ischemic mice. Male C57BL/6 mice were subjected to middle cerebral
artery occlusion (MCAO) and reperfusion. EPO (5000 U/kg), MEPO (5000
U/kg) or equal volume of normal saline was injected intraperitoneally.
Neurological function was evaluated by Rota-rod test, Neurological
severity scores (NSS) and Adhesive removal test. After ischemia and
reperfusion (I/R), the survival rate, brain tissue loss, neurogenesis,
angiogenesis and gliogenesis were detected by Nissl staining,
Immunofluorescence and Western blot, respectively. The results shown
that MEPO significantly increased survival rate, reduced brain tissue
loss, and improved neurological function after MCAO (P<0.05).
Furthermore, MEPO obviously enhanced the proliferation of neuronal
precursors (DCX) and promoted its differentiation into mature neurons
(NeuN) (P<0.05). In addition, compared to normal saline
treatment mice, MEPO increased the number of BrdU-positive cells in the
cerebral vasculature (P<0.05). Whereas, MEPO treatment also reduced the numbers of newly generated astrocytes (GFAP) and microglia (Iba1) (P<0.05).
Among all the tests in this study, there was no significant difference
between EPO group and MEPO group. Taken together, MEPO promoted the
regeneration of neurons and blood vessels in peripheral area of
infarction, and suppressed the gliogenesis, thus promoting neurogenesis,
improving neurological function and survival rate. Our findings suggest
that the MEPO may be a therapeutic drug for ischemic stroke
intervention.
So your doctors, stroke hospital and stroke association should followup with
human research testing this out. That is the minimum a competent doctor, stroke hospital and stroke association should be doing. But you already know that nothing will be done unless you do this testing yourself. Hope you don't die. You would be in good company;
Mouse study reverses memory loss in mice with Alzheimer’s.
Memory loss caused by Alzheimer’s disease has been reversed in mice, reports a new study.
Alzheimer’s disease — the most common form of dementia –results from
both genetic and environmental factors, and is currently untreatable.
Scientists have discovered, though, that the disease interferes with
electrical signalling in part of the brain responsible for memory.
Using techniques based on epigenetics, the researchers were able to reverse the memory loss.
Epigenetics involves how instructions contained in DNA are expressed in cells.
Professor Zhen Yan, the study’s first author, said:
“We have not only identified the epigenetic factors that
contribute to the memory loss, we also found ways to temporarily reverse
them in an animal model of AD.”
The scientists found that Alzheimer’s caused neurons in the frontal cortex to gradually lose glutamate receptors.
By inhibiting an enzyme, they were able to restore memory in mice.
Professor Yan said:
“When we gave the Alzheimer’s animals this enzyme
inhibitor, we saw the rescue of cognitive function confirmed through
evaluations of recognition memory, spatial memory and working memory.
We were quite surprised to see such dramatic cognitive improvement.
At the same time, we saw the recovery of glutamate receptor expression and function in the frontal cortex.”
While the drug only worked on the mice for one week, it is hoped the method can be refined to make it more powerful.
Epigenetics is powerful because it can target the effects of more than one gene, said Professor Yan:
“An epigenetic approach can correct a network of genes,
which will collectively restore cells to their normal state and restore
the complex brain function.
We have provided evidence showing that abnormal epigenetic regulation
of glutamate receptor expression and function did contribute to
cognitive decline in Alzheimer’s disease.
If many of the dysregulated genes in AD are normalized by targeting
specific epigenetic enzymes, it will be possible to restore cognitive
function and behavior.”
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