Use the labels in the right column to find what you want. Or you can go thru them one by one, there are only 34,483 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. Did your doctor somehow miss the recovery protocol that Pedro Bach-y-Rita used to recover fully back in 1958 with only a partial brain?
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.
You're living in la-la land if you think this has become a protocol at your stroke hospital. Ask the question, and not politely. So far 1 year to accomplish this. Is your hospital a failure?
Objectives:
The 2024 American Heart Association and American Stroke
Association stroke prevention guideline newly recommended glucose-like
peptide-1 receptor agonists (GLP-1s) for primary prevention of stroke in
patients with diabetes and elevated risk of atherosclerotic
cardiovascular disease (ASCVD). We aimed to characterize the population
newly recommended GLP-1s.
Methods:
This cross-sectional study included adults aged 30-79 years
without previous stroke and with diabetes who participated in the
National Health and Nutrition Examination Survey from 2017 to March
2020. Participants were guideline-eligible for GLP-1 if they had HbA1C
≥7% and existing or a high 10-year risk of ASCVD. Current GLP-1 users
were identified by in-home review of medications. Data were weighted to
be nationally representative.
Results:
The study included 1,104 participants (mean age 60 years; 45%
female) representing 23.5 million (95% CI, 21.2 million-25.8 million) US
adults with diabetes. Stroke prevention guideline recommendations would
apply to 4.9 million (95% CI, 3.7 million-6.0 million) US adults. GLP-1
eligibility was more common among older adults, men, and those with
private insurance or Medicare. Only 6.8% (95% CI 3.3%-10.7%) of adults
meeting recommendations were taking a GLP-1.
Discussion:
Almost 5 million Americans with diabetes would qualify for GLP-1
use for primary prevention of stroke, but current use among this
population is very low.
Liraglutide may improve outcomes and prognosis after minor stroke/transient ischemic attack in patients with diabetes.
However, the trial was halted prematurely and the data should be interpreted with caution.
The GLP-1 liraglutide showed potential benefit in reducing stroke
recurrence and improving functional outcomes after minor stroke or
transient ischemic attack, a speaker reported.
However, the LAMP study, presented at the International Stroke
Conference, was terminated early due to slow enrollment and cost.
Data were derived from Zhu H, et al. LB44. Presented at:
International Stroke Conference; Feb. 5-7, 2025; Los Angeles (hybrid
meeting).
“Diabetes increases the [incidence] and recurrence of stroke by two to four times.
But insulin or sulfonylurea-based treatment for glycemic control did
not reduce the risk of microvascular complications such as myocardial
infarction and ischemic stroke. Even with 3 weeks of dual antiplatelet
therapy, 12.8% of diabetic patients with minor acute ischemic stroke
experienced recurrence within 90 days,” Hui-LiZhu, MD,
associate professor at The First Affiliated Hospital of Jinan
University, Guangzhou, China, said during a presentation. “Liraglutide
is a synthetic long-acting GLP-1 receptor agonist, and has the ability
to cross the blood-brain barrier. Our previous study showed liraglutide
decreased the infarct volume and improved neurologic deficits in a rat
model of [middle cerebral artery] occlusion. ... Both basic research and
clinical studies have suggested that GLP-1 receptor agonists may have the potential to improve stroke recurrence and prognosis.”
LAMP was a multicenter, randomized controlled, prospective trial
designed to evaluate the efficacy and safety of liraglutide
(Victoza/Saxenda, Novo Nordisk) for the prevention of recurrent stroke
after minor ischemic stroke or high-risk TIA in patients with diabetes.
The LAMP study was terminated early due to a lower-than-expected
enrollment and financial constraints, which prevented completion within
the planned timeframe or target sample size, according to the
presentation.
Overall, 636 patients hospitalized with minor ischemic stroke or
high-risk TIA within 24 hours of symptom onset were included in the
study and were randomly assigned to liraglutide or usual care.
Individuals assigned to liraglutide were provided ascending daily
doses of the drug, starting with 0.6 mg and rising to 1.8 mg by day 30.
The primary endpoint was occurrence of new strokes within 90 days of index stroke.
Baseline characteristics were balanced between the liraglutide and
usual care groups (mean age, 64 years; 36% women; 91% with history of
diabetes; mean baseline HbA1c, 8.2%). The average BMI was approximately
24 kg/m2and one-third of patients were currently smoking.
Subsequent new stroke occurred in 13.8% of the usual care arm
compared with 7.9% of the liraglutide arm, which in the
intention-to-treat analysis translated to a hazard ratio of 0.56
favoring liraglutide (95% CI, 0.34-0.91; P = .02). However, due to insufficient sample size, statistical power was only 67%.
In secondary analysis, the researchers reported that after minor
ischemic stroke or high-risk TIA, individuals with diabetes assigned to
liraglutide were more likely to achieve a modified Rankin score of 1 or
less at 90 days compared with usual care (OR = 1.95; 95% CI, 1.28-3; P
= .002). Similarly, liraglutide was associated with greater likelihood
to achieve a modified Rankin score of 2 or less compared with usual care
(OR = 1.77; 95% CI, 1.06-3.02; P = .032).
“Among Chinese patients with minor acute ischemic stroke or high-risk
TIA who were diagnosed with type 2 diabetes, treatment with liraglutide
probably reduced the risk of stroke recurrence and improved outcomes at
90 days,” Zhu said during the presentation. “Careful interpretation of
these early terminated study results is warranted, and additional
research is required to confirm these potential benefits. The LAMP study
is the first and largest-scale trial investigating GLP-1 receptor
agonists in patients with ischemic stroke, offering some valuable
insights into their potential benefits for improving patient outcomes.”
So you didn't put together EXACT PROTOCOLS to push to stroke hospitals. You really think stroke hospitals will use this information to get survivors recovered? Then you're living in la-la land.
A
modern and accessible healthcare system requires digital innovation and
connectivity. The term “Digital health” covers vide range technologies,
such as mobile health and applications, electronic records, telehealth
and telemedicine, wearable devices, robotics, virtual reality and
artificial intelligence.
Methods
Scientometrics
is the method that we have done in this study by Cite Space and
VOSviewer software, and the result of searching the Web of Science
database in plain text format to perform analysis and scientometrics and
create outputs in the form of graphs and tables in the field of digital
health has been used in stroke rehabilitation.
Result
A
total of 2933 documents related to digital health technologies in
stroke rehabilitation were identified by searching for the terms “stroke
rehabilitation” or “stroke recovery” in the title and “digital health”
across all fields. The strongest citations related to cerebrovascular
disease spanned from 1994 to 2007, with randomised clinical trials
occurring almost simultaneously and ended by 2012. Consequently, stroke
rehabilitation by virtual reality technology has obtained the most
citations and clinical trials and as an important part of digital health
in the future research process.
Conclusion
This
scientometric study offers insights into how digital health technology
can assist stroke patients in self-managing their health and well-being,
in addition to supporting integrated stroke rehabilitation. The
analysis revealed that three themes were present: author contributors
and collaboration networks, temporal evolution, the strongest citation
explosions for digital health technologies in stroke rehabilitation
research, and semantic analysis.
IMPLICATIONS FOR REHABILITATION
The new technology for helping stroke patients get better is a big help to many people with health problems.
Newer
technologies are now more common, and more patients are using remote
health care monitoring. We need to do more research to figure out if
these digital health technologies work well over a long period of time.
This
study connects digital technology and stroke rehab research. It looks
at different research areas and trends, and gives a wider view than
other similar studies. The findings show where more research should be
done and help researchers work together in different areas to improve
our knowledge of stroke rehabilitation.
Do you really think your stroke hospital has an employee whose only job is to follow research and create protocols to treat their patients? Or to get further research done in humans? Then you are in la-la land.
Researchers at Case
Western Reserve University School of Medicine say they have identified a
previously unknown gene and associated protein that could potentially
be suppressed to slow the advance of Alzheimer’s disease.
“Based on the data we have, this protein can be an unrecognized new risk factor for Alzheimer’s disease (AD),” said Xinglong Wang,
an associate professor of pathology at the School of Medicine. “We also
see this as a potential novel therapeutic target for this devastating
disease.”
Xinglong Wang
Wang said proving the latter
assertion, which has not yet been tested in humans, would require additional
research to corroborate the function of the protein they have dubbed “aggregatin.”
Eventually, that would someday mean clinical trials with
Alzheimer’s patients, he said.
“This protein characteristically accumulates, or aggregates, within
the center of plaque in AD patients, like the yolk of an egg—which is
part of the reason we named it ‘aggregatin,’” Wang said.
A research team led by Wang and Xiaofeng Zhu,
a professor of population and quantitative health sciences at the
School of Medicine, has filed for a patent through the university’s
Office of Research and Technology Management for “novel Alzheimer’s
disease treatments and diagnosis based on this and related study,” Wang
said.
Xiaofeng Zhu
“We’re very excited about this because our study
is likely the first systematic work combining the identification from a genome-wide
association study of high dimensional brain-imaging data and experimental
validation so perfectly in Alzheimer’s disease,” Zhu said.
More than 5.7 million Americans have Alzheimer’s disease,
which is the primary cause of dementia and sixth-leading cause of death in the
United States. That population is predicted to reach 14 million by the year
2050, according to the Alzheimer’s Association.
The relationship between Alzheimer’s (and subsequent
brain atrophy) and amyloid plaques—the hard
accumulations of beta amyloid proteins
that clump together between the nerve cells (neurons) in the brains of
Alzheimer’s patients—has been well-established among researchers.
Less understood is precisely how that amyloid-beta actually
leads to plaque formation—and where this new work appears to have broken new
ground, Wang said.
Further, while there has been much research
into what genes might influence whether or not someone gets Alzheimer’s, there
is less understanding of genes that might be linked to the progression of the disease, meaning the formation of plaque and
subsequent atrophy in the brain.
The
role of ‘aggregatin’ protein
An image of the ‘Aggregatin’ protein from the paper published by Wang, Zhu and collaborators.
In the new work, the researchers began by correlating
roughly a million genetic markers (called single-nucleotide polymorphisms, or SNPs)
with brain images. They were able to identify a specific SNP in the FAM222, a
gene linked to different patterns of regional brain atrophy.
Further experiments then suggested that the
protein encoded by gene FAM222A is not only associated with AD patient-related
beta-amyloid plaques and regional brain atrophy, but that “aggregatin” attaches
to amyloid beta peptide—the major component of plaque and facilitates the plaque
formation.
So when researchers injected mouse models with
the “aggregatin” protein (made from the FAM222A gene), plaque
(amyloid deposits) formation accelerated in the brain, resulting in more neuroinflammation
and cognitive dysfunction. This happened, they report, because the protein was
found to bind directly the amyloid beta peptide, thus facilitating the
aggregation and placque formation, Wang said.
Conversely, when they suppressed the protein, the plaques
were reduced and neuroinflammation and cognitive impairment alleviated.
Their findings indicate that reducing levels of this
protein and inhibition of its interaction with amyloid beta peptide could
potentially be therapeutic—not necessarily to prevent Alzheimer’s but to slow its
progression.
For more information, contact Mike Scott at mike.scott@case.edu
