Use the labels in the right column to find what you want. Or you can go thru them one by one, there are only 29,372 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.
I've tried a couple of times to get spasticity out of my fingers. Failure on all counts!
Failure number 1:
I received the godawful hand built blue plastic hand and wrist
splint for nighttime use that rotted after 3 years and never managed to
keep my fingers straight no matter how I tried velcroing them down.
Benik w-700 hand splint:
It is pretty much impossible to put on one-handed, but this should have been given in the hospital to prevent spasticity in the hand from changing to contractures.
How to heat it first, then putting it on, one handed by yourself is quite difficult.
By stopping the 5 causes of the neuronal cascade of death in the first week you could save hundreds of millions to billions of neurons thus possibly preventing this problem!
The ability to follow instructions and its impact on the
rehabilitation of stroke patients has never been investigated — until
now.
Researchers at the Joint Laboratory for Neurological Rehabilitation
Research of Ben-Gurion University of the Negev and Adi-Negev Nahalat
Eran have explored the science of following instructions and patients’
motor recovery.
Their findings were published in the journal Neuropsychology.
Every day we use our ability to understand instructions for routine
daily activities. But what happens to stroke survivors with impairments
that affect this ability?
Dr. Reut Binyamin-Netser and Prof. Lior Shmuelof from the Department
of Cognitive and Brain Sciences at Ben-Gurion University of the Negev
examined how stroke affects the ability to follow changing instructions
and what cognitive abilities underlie this ability.
Stroke occurs because of a sudden disruption in the blood supply to
brain tissue by a blood clot or by bleeding. This disruption causes
neuronal damage that can manifest in various ways.
One of the most common impairments (72 percent of cases) after stroke is cognitive impairment.
Cognitive impairment manifests in memory and attention problems and
in impairments in abilities that require executive functions, adaptation
processes to change, adjustments to unexpected situations, and
self-control. These impairments lead to functional deficits and predict a
lower chance of independent functioning after stroke.
Another consequence of cognitive impairment after stroke is
impairment in the learning ability of subjects, which may affect their
ability to participate in and benefit from the rehabilitation treatment
they receive.
To investigate the phenomenon, the researchers examined two groups of
subjects. One group consisted of 31 stroke patients, while 36 subjects
in the same age range (55-75) served as a control group. All
participants in the study were given computerized tasks in which they
had to respond to stimuli according to their color and location on the
screen, and other tasks designed to characterize cognitive abilities
such as response inhibition ability and information processing speed
using symbols.
The results showed a decrease in accuracy and response times during
instruction following a stroke (compared to the control group). In
addition, there was a decrease in information processing speed and a
decrease in response inhibition ability. A relationship was also found
between the patients’ response inhibition abilities and their ability to
follow instructions.
“Response inhibition ability affects the ability of patients to
participate in the rehabilitation process,” explained Dr.
Binyamin-Netser. “Understanding instructions and tasks is also the basis
for motor rehabilitation since the process is a product of
instruction.”
“The study opens the door to examining the relationship between
cognitive functions and motor and cognitive recovery,” Professor
Shmuelof said. “This connection is critical in an era where technologies
such as video games play a central role in rehabilitation.”
The researchers recommend starting an intensive rehabilitation
program using computerized technologies as early as possible to improve
the stroke recovery process.
“The cognitive ability of the patient is critical to the success of
such interventions. Improving motor and cognitive rehabilitation are
intertwined, so understanding instructions is the basis for the entire
process,” Dr. Binyamin-Netser added.
Anat Shaked Ravni, an engineer from the Department of Cognitive and
Brain Sciences at Ben-Gurion University of the Negev, also participated
in the study. The research was supported by the Israel Science
Foundation ((grant number 1244/22), the Marcus Foundation (Ben-Gurion
University of the Negev) and Adi Negev.
Stroke is a sudden neurological illness that results in various abnormalities in the brain
region. Paresis, spasticity, and alterations in the muscular activation sequence are all symptoms of a
stroke, resulting in impairment. These immediate effects of stroke impact activity and may limit a
person's engagement.
Aim:
The behavioural and neuro physiological alterations associated with two such rehabilitation
procedures, bilateral and unilateral movement therapy, were compared in this research. This
research aimed to see how functional unilateral vs. bilateral motor recovery and training affected
upper limb function.
Method:
Scores on the FMSA Fugl-Meyer Scale Assessment (separated into distal and proximal
subscales) before and after therapy scales are used to measure involvement, activity, and motor
function, respectively, before and after treatment. Thirty chronic stroke patients were allocated to
control and two training procedures, including six months of daily practice sessions.
Result:
At the baseline, there was a significant distinction between the two groups. Compared to the
control group, the bilateral treatment group demonstrated substantial improvements in FMA test
after the training sessions. Compared to people who received unilateral instruction, those who
received bilateral training demonstrated a reduction in movement time of the damaged arm and an
improvement in capacity of upper limb function.
Conclusion:
Overall, our data imply that a short-term bilateral hand training intervention might help(WHOM will do the research that changes this to WILL RECOVER?)
chronic stroke patients regain upper limb motor function. Unilateral and bilateral, both motor
How will your competent? doctor use this to ensure your brain isn't aging inappropriately? OH, DOING NOTHING! So, you DON'T have a functioning stroke doctor, do you?
Summary: New research shows that not all brain cells
age equally, with certain cells, such as those in the hypothalamus,
experiencing more age-related genetic changes. These changes include
reduced activity in neuronal circuitry genes and increased activity in
immunity-related genes.
The findings provide a detailed map of
age-sensitive brain regions, offering insights into how aging may
influence brain disorders like Alzheimer’s. This research could guide
the development of treatments targeting aging-related brain changes and
neurodegenerative diseases.
Key Facts:
Uneven Aging: Hypothalamic neurons and ventricle-lining cells show the greatest age-related genetic changes.
Therapeutic Potential: Mapping age-sensitive cells may inform treatments for aging-related brain diseases.
Source: NIH
Based on new brain mapping
research funded by the National Institutes of Health (NIH), scientists
have discovered that not all cell types in the brain age in the same
way.
They found that some cells, such as a small group
of hormone-controlling cells, may undergo more age-related changes in
genetic activity than others.
The results, published in Nature, support the idea that some cells are more sensitive to the aging process and aging brain disorders than others.
Like
previous studies, the initial results showed a decrease in the activity
of genes associated with neuronal circuits. Credit: Neuroscience News
“Aging is the most important risk factor for Alzheimer’s disease and
many other devastating brain disorders. These results provide a highly
detailed map for which brain cells may be most affected by aging,” said
Richard J. Hodes, M.D., director of NIH’s National Institute on Aging.
“This
new map may fundamentally alter the way scientists think about how
aging affects the brain and also provide a guide for developing new
treatments for aging-related brain diseases.”
Scientists used
advanced genetic analysis tools to study individual cells in the brains
of 2-month-old “young” and 18-month-old “aged” mice.
For each age,
researchers analysed the genetic activity of a variety of cell types
located in 16 different broad regions — constituting 35% of the total
volume of a mouse brain.
Like previous studies, the initial results showed a decrease in the activity of genes associated with neuronal circuits.
These
decreases were seen in neurons, the primary circuitry cells, as well as
in “glial” cells called astrocytes and oligodendrocytes, which can
support neural signaling by controlling neurotransmitter levels and
electrically insulating nerve fibers.
In contrast, aging increased the activity of genes associated with
the brain’s immunity and inflammatory systems, as well as brain blood
vessel cells.
Further analysis helped spot which cell types may be
the most sensitive to aging. For example, the results suggested that
aging reduces the development of newborn neurons found in at least three
different parts of the brain.
Previous studies have shown that
some of these newborn neurons may play a role in the circuitry that
controls some forms of learning and memory while others may help mice
recognize different smells.
The cells that appeared to be the most
sensitive to aging surround the third ventricle, a major pipeline that
enables cerebrospinal fluid to pass through the hypothalamus.
Located
at the base of the mouse brain, the hypothalamus produces hormones that
can control the body’s basic needs, including temperature, heart rate,
sleep, thirst, and hunger.
The
results showed that cells lining the third ventricle and neighbouring
neurons in the hypothalamus had the greatest changes in genetic activity
with age, including increases in immunity genes and decreases in genes
associated with neuronal circuitry.
The authors noted that these observations align with previous studies
on several different animals that showed links between aging and body
metabolism, including those on how intermittent fasting and other
calorie restricting diets can increase life span.
Specifically,
the age-sensitive neurons in the hypothalamus are known to produce
feeding and energy-controlling hormones while the ventricle-lining cells
control the passage of hormones and nutrients between the brain and the
body.
More research is needed to examine the biological
mechanisms underlying the findings, as well as search for any possible
links to human health.
The project was led by Kelly Jin, Ph.D.,
Bosiljka Tasic, Ph.D., and Hongkui Zeng, Ph.D., from the Allen Institute
for Brain Science, Seattle. The scientists used brain mapping tools —
developed as part of the NIH’s Brain Research Through Advancing Innovative Neurotechnologies® (BRAIN)
Initiative – Cell Census Network (BICCN) — to study more than 1.2
million brain cells, or about 1% of total brain cells, from young and
aged mice.
“For years scientists
studied the effects of aging on the brain mostly one cell at a time.
Now, with innovative brain mapping tools – made possible by the NIH
BRAIN Initiative – researchers can study how aging affects much of the
whole brain,” said John Ngai, Ph.D., director, The BRAIN Initiative®.
“This study shows that examining the brain more globally can provide
scientists with fresh insights on how the brain ages and how
neurodegenerative diseases may disrupt normal aging activity.”
Funding: This study was funded by NIH grants R01AG066027 and U19MH114830.
About this aging and brain mapping research news
Author: Christopher Thomas Source: NIH Contact: Christopher Thomas – NIH Image: The image is credited to Neuroscience News
Artificial intelligence is completely useless until we get EXACT 100% RECOVERY PROTOCOLS CREATED! Are you that blitheringly stupid you can't see that? You're using the tyranny of low expectations to ignore what survivors want!
Since the goal of all stroke survivors is 100% recovery this is putting the cart before the horse! What fucking stupidity!
Send
me hate mail on this: oc1dean@gmail.com. I'll print your complete
statement with your name and my response in my blog. Or are you afraid
to engage with my stroke-addled mind? I would like to know why you
aren't solving stroke to 100% recovery, and what is your definition of
competence in stroke? Swearing at me is allowed, I'll return the favor.
The technological revolution driven by advancements in Artificial Intelligence (AI) is radically transforming various sectors, with healthcare among the most positively impacted. This article is situated within the context of such transformation, highlighting the contribution of AI in supporting professionals dedicated to the physical rehabilitation of stroke survivors. Our study focuses on the design of a Decision Support System (DSS) integrated within a comprehensive remote rehabilitation framework, consisting of two interconnected applications: one for the therapist, designed to define routines and monitor patients, and another for the patient, enabling autonomous rehabilitation exercises at home. This DSS employs fuzzy logic, significantly enhancing its scalability and interpretability. We propose a system capable of automatically suggesting personalized adjustments to a patient’s rehabilitation routine based on their performance. Our approach can offer physiotherapists considerable time savings by automating routine adjustments, thereby allowing them to allocate more attention to personalized patient care and complex case analysis. Furthermore, this system incorporates principles of Artificial Intelligence (XAI), providing justifications for its suggestions. This affords therapists a stronger basis for validating or rejecting the proposed modifications by the artificial system. The paper presents a case study where a stroke patient’s rehabilitation routine is automatically adjusted by the system, demonstrating the applicability and benefits of our approach. The routine generated by the artificial system is compared with the routine that a physiotherapist could potentially assign and modify manually when monitoring the progress of a stroke patient. Finally, the findings of a preliminary evaluation with patients and therapists in a hospital are also discussed.
Accelerated brain aging is a risk factor for dementia, and resilience to normal brain aging is associated with cognitive preservation. Liu and colleagues explore plasma proteomic changes associated with brain aging and identify peaks of brain aging-related protein changes in middle-aged or older adults.
To
investigate the cost-effectiveness of a cardiac rehabilitation program
in individuals with stroke compared with customary care.
Design
A
Markov model was created using a 30-year time horizon, with cycle
lengths of 1 year to determine the effectiveness and cost-effectiveness
of a cardiac rehabilitation program in persons with stroke. Input
parameters were based on recently published literature. Health states
were defined as degree of disability evaluated by the modified Rankin
scale score. Costs were based on recent cost-effectiveness analyses and
inflated to 2024 US Dollars using the medical care component of the US
Consumer Price Index.
Setting
Outpatient ambulatory setting
Participants
Persons with mild disability after ischemic stroke
Intervention
A model comparing cardiac rehabilitation versus usual care was created.
Main Measures
Quality-adjusted
life years (QALYs) were used to measure the effectiveness of cardiac
rehabilitation versus usual care. The cost-effectiveness of cardiac
rehabilitation versus usual care was compared with respect to
incremental costs, incremental effectiveness, and incremental
cost-effectiveness ratios (ICERs).
Results
Cardiac
rehabilitation was the superior strategy, resulting in higher
incremental effectiveness of 3.28 QALY at an increased incremental cost
of $5704. The ICER was $1740/QALY. A two-way sensitivity analysis of
these variables had no change, with cardiac rehab remaining the optimal
strategy.
Conclusions
While
numerous studies and systematic analyses have reported compelling
evidence of the clinical benefits of cardiac rehabilitation for patients
with stroke, the current study contributes to the existing body of
literature, demonstrating that cardiac rehabilitation is also
cost-effective in the stroke population.
Ask your competent? doctor if any of these devices have gone from 'may improve' to WILL IMPROVE! 8 years and your doctor STILL DOESN'T KNOW THE ANSWER!
How fucking incompetent can you be and still be employed?
Jacob Brackenridge 1 , Lynley V. Bradnam 2,3 , Sheila Lennon 2 , John J. Costi 1 and David A. Hobbs 1, * 1 Medical Device Research Institute, School of Computer Science, Engineer- ing and Mathematics, Flinders University, Adelaide, South Australia, Australia; 2 Discipline of Physiotherapy, School of Health Sciences, Flinders University, Adelaide, South Australia, Australia; 3 Discipline of Physiotherapy, Graduate School of Health, University of Technology, Sydney, NSW, Australia
Neuroscience and Biomedical Engineering, 2016, 4, 25-42
Abstract:
Background:
Stroke is a major contributor to the reduced ability to carry out activities of daily living (ADL) post cerebral infarct. There has been a major focus on understanding and improving rehabilitation interventions in order to target cortical neural plasticity to support recovery of upper limb function. Conventional therapies delivered by therapists have been combined with the application of mechanical and robotic devices to provide controlled and assisted movement of the paretic upper limb. The ability to provide greater levels of intensity and reproducible repetitive task practice through the application of intervention devices are key mechanisms to support rehabilitation efficacy.
Results:
This review of literature published in the last decade identified 141 robotic or mechanical devices. These devices have been characterized and assessed by their individual characteristics to provide a review of current trends in rehabilitation device interventions. Correlation of factors identified to promote positive targeted neural plasticity has raised questions over the benefits of expensive robotic devices over simple mechanical ones.
Conclusion:
A mechanical device with appropriate functionality to support the promotion of neural plasticity after stroke may provide an effective solution for both patient recovery and to stimulate further research into the use of medical de- vices in stroke rehabilitation. These findings indicate that a focus on simple, cost effective and efficacious intervention solutions may improve rehabilitation outcomes.
Roughly a fourth of the Indian population has access to a rehabilitation centre within an hour of experiencing an ischaemic stroke -- caused when a blood clot affects supply to the brain, a study has found. The research, published in the International Journal of Stroke, also estimated that there is less than one ischaemic stroke centre per million population.
Ischaemic stroke is the most common, accounting for about 70-80 per cent of all strokes in India, according to a September 2024 study, published in the journal Scientific Reports.
In the recent study, researchers, including those from the US' Ascension Health and All India Institute of Medical Sciences (AIIMS), Hyderabad, found that a total of 566 stroke centres equipped with the 'intravenous thrombolysis method of treatment (which breaks up blood clots) were spread across 26 states and union territories.
Of the 566, over 60 per cent (361) were found to be also equipped with endovascular therapy for stroke patients, considered superior.
Typically, an ischaemic stroke patient was 115 kilometres away from the nearest intravenous thrombolysis treatment centre and about 130 kilometres away from the nearest endovascular therapy centre, the researchers found.
Further, a little over 26 per cent of the Indian population can access intravenous thrombolysis centre in under an hour, while about a fifth can access endovascular therapy centre, the team found.
For the analysis, data on "intravenous thrombolysis capable (IVT-C) and endovascular treatment capable (EVT-C)" stroke centres were collected in March 2021 from medical devices and pharmaceutical industry providers. Time taken to drive to the nearest stroke care centre was estimated using the application 'Google Distance Matrix API'.
"Access within one hour to an IVT-C and an EVT-C centre was available to 26.3 per cent and 20.6 per cent of the Indian population, respectively," the authors wrote.
"The average stroke centres per million (SCPM) population was 0.41 and 0.26 for IVT-C and EVT-C, respectively," they wrote.
Further, "median (typical) distances to the nearest IVT-C and EVT-C centres were 115 kilometres and 131 kilometres, respectively."
The authors said establishing stroke facilities equipped with intravenous thrombolysis and endovascular treatments in poorly served regions in India(Which won't get them 100% recovered! That is the only goal for all stroke survivors, if you would listen to their requirements!) is urgently needed to increase access and improve outcomes for stroke patients.
Roughly
a fourth of the Indian population has access to a rehabilitation centre
within an hour of experiencing an ischaemic stroke -- caused when a
blood clot affects supply to the brain, a study has found. The research,
published in the International Journal of Stroke, also estimated that
there is less than one ischaemic stroke centre per million population.
Roughly
a fourth of the Indian population has access to a rehabilitation centre
within an hour of experiencing an ischaemic stroke -- caused when a
blood clot affects supply to the brain, a study has found. The research,
published in the International Journal of Stroke, also estimated that
there is less than one ischaemic stroke centre per million population.
Roughly
a fourth of the Indian population has access to a rehabilitation centre
within an hour of experiencing an ischaemic stroke -- caused when a
blood clot affects supply to the brain, a study has found. The research,
published in the International Journal of Stroke, also estimated that
there is less than one ischaemic stroke centre per million population.
If you’re a runner, there’s a good chance you might be training for an upcoming race or just looking to increase how quickly you can cruise around your neighborhood during a run.
Your need for speed probably includes tracking your stats (What is your RPE? What should your weekly mileage be?) and thinking about all the different ways to be faster (Are your shoes lightweight? Should you add sprints into your routine?).
And while there are several methods and strategies when it comes to running, have you considered running slower?
Similar
to how it feels to jog, the idea behind “slow running” (also known as
low-intensity running) is that by slowing your pace, you can log more
run miles and train your body in a variety of ways, such as building
your endurance, strengthening your muscles, heart and lungs.
“There’s a lot of evidence to show the incredible aerobic changes we can have with slow running,” says cardiologist Tamanna Singh, MD.
Dr. Singh, a runner herself, shares the benefits of slow running and gives us some tips on how to slow run.
What is slow running?
“The
best way to identify slow running is to equate it to a subjective
sensation of a jog. A jog is a perfect way to visualize a run where
you’re very easily carrying a conversation. There’s no huffing and
puffing between two or three words. If you wanted to sing to a song
you’re listening to while you’re running, you could,” says Dr. Singh.
“It’s an effort that you could sustain essentially forever.”
What slow running means in terms of speed and pace is different for each runner.
“For
example, for someone who typically runs an 18- to 20-minute 5K, their
slow pace is going to still be a little faster than someone who perhaps
runs at a 25- to 30-minute 5K pace,” she adds.
When
you finish your slow run, you may even feel like you can keep going
instead of feeling tired and out of breath like you would on a normal
run. Your slow run should feel comfortable and not too challenging.
The
idea isn’t to completely stop pushing yourself on runs. It’s more about
being strategic with your training. You want to have a good mix of
intensity — most runs should be slow, while other runs should be where
you push yourself to run fast.
A good rule of thumb? About 80% of your runs should be slow running and the other 20% should be faster.
“It depends on what you’re training for, your running experience and your injury experiences,” clarifies Dr. Singh.
And if you’re someone who tracks their heart rate zones, Dr. Singh says that you want to stay in zone two for the majority of your run.
“Zone two running is basically usually around 55% to 65% of your max predicted heart rate.”
Benefits of slow running
Not sold on the idea that slow running will help you train for that upcoming race or to just increase how fast you run?
Slow running benefits include:
Builds your endurance.
Adapts joints, ligaments, tendons and bones to stress from running.
Sure, you might be able to run a nine-minute mile right now, but can you keep that pace up for five miles or 10 miles?
By incorporating slow running into your routine, you can improve your stamina and resistance to fatigue.
And
that’s thanks to improving your mitochondria function. Mitochondria can
be found in almost every cell in your body and produces 90% of your
body’s energy. Mitochondria process oxygen and convert food into energy.
“We can increase mitochondrial density by running slowly, running aerobically,”
explains Dr. Singh. “We can also develop capillary beds or beds of
little blood vessels, which then help us increase the amount of oxygen
delivery to your muscles. By improving oxygen delivery or essentially
increasing the energy that you can deliver, you’re able to increase the
time between the start of your run and the timing of fatigue.”
While
slow running helps with your endurance, it also helps retrain your
muscle fibers. If you run longer distances, your body needs to be able
to sustain that effort. By strengthening your muscles through slow
running, you’ll be able to maintain a faster pace for a longer time.
For example, say your slow runs are around a 10-minute mile pace. During those runs, you can easily sing your favorite song.
“Building the endurance and the cardiac efficiency
is what helps you then start to slowly get a little faster on your slow
runs,” says Dr. Singh. “What you’ll notice over time — and it’s not
over a couple of days or a couple of weeks, but over the course of a
couple of months or up to a year — you’ll notice that your slow pace is
faster than the prior 10 minutes per mile.”
And the idea is that by incorporating slow running into your training, you’re less likely to sustain injuries.
“If
you watch people sprinting compared to someone who’s jogging, you can
visibly see the change and the difference in impact of the foot to the
ground,” she continues. “The amount of power you need in your legs and
the force of impact is going to be far greater if you’re sprinting or
running fast versus if you’re running slow.”
Over time, that wear and tear on your body can take a toll.
“The
demands on the body are much higher, the risk of injury is much higher
the faster you go,” notes Dr. Singh. “Slow running will help you stay
healthy for longer. There’s a place for fast efforts and a place for
learning how to run fast and how to train your muscles to run fast. But
there’s space for keeping miles easy to protect yourself from injury.”
Tips for slow running
“The
first thing you need to do is throw your ego out the window. That’s the
hard part,” relates Dr. Singh. “It’s going to freak you out how slow
you’re going. One way to think about it is don’t even think about it as
slow running. Tell yourself the purpose of this run is to increase your
mitochondrial density, the purpose of this run is to improve your
efficiency, the purpose of this run is to improve and enhance the
ability for you to deliver oxygen to your legs when you’re running.”
Here are some other slow running tips:
Ignore your watch.
You probably use a smartwatch to track all kinds of data related to
your health. “Just remember that your body is what is giving the
feedback to your watch — it’s not the other way around,” stresses Dr.
Singh. “So, if your watch is giving you anxiety, if looking down at your
pace is causing you to have freak-out moments, leave your watch at
home.”
Have a run buddy. “It can be incredibly helpful, especially if you and your buddy run at similar paces,” says Dr. Singh. “Set your intentions: We’re going to catch up on what’s been going on this week.
I think that’s a phenomenal way to learn and understand what slow
running is. And time flies when you’re having a good conversation.”
Set your intentions.
Start out each run thinking about what you want to accomplish.
“Sometimes, I’ll focus on running a specific amount of time versus a
specific number of miles,” says Dr. Singh. “That takes the stress out of
getting a certain number of miles, which means I won’t try to run
faster to get the mileage done.”
Bottom line?
Looking for a personal testimony on how slow running can change your run game? Look no further than Dr. Singh.
“I
have become much faster after incorporating slow running to the point
where one of my buddies who I run with, who perhaps doesn’t really
subscribe to the slow running idea, has said they can’t believe how much
I’ve improved my run time,” she shares.
So, consider slow running and how it can play a part in your running routine and strategy.
“If
you want to become a faster runner, remember that Rome wasn’t built in a
day and your goal pace isn’t going to be built in a day,” says Dr.
Singh. “But the time you spend in optimizing your body and the
biological mechanics within your body are really going to help you in
the long run.”
he American College of Cardiology (ACC)
recently published a new expert consensus document on practical
approaches for arrhythmia monitoring after stroke. The guidance offers
clinicians tailored strategies to improve post-stroke care by
identifying and managing atrial fibrillation (AF) and other arrhythmias
linked to recurrent stroke risk.
The ACC Solution Set Oversight Committee's "2024 ACC Expert Consensus Decision Pathway on Practical Approaches for Arrhythmia Monitoring After Stroke"
includes comprehensive guidance for arrhythmia detection based on
stroke subtype, leveraging extended monitoring and implantable cardiac
monitors where appropriate.[1] The document offers a detailed evaluation
of medical-grade and consumer-grade monitoring devices to support
clinicians in selecting the right tools for individual patients. The
document also emphases collaboration between clinicians and patients to
personalize monitoring strategies and treatment plans.
“There
is growing consensus on the role of cardiac rhythm monitoring in
patients after a stroke that is informed by outcomes of several recent
landmark trials,” said Michael T. Spooner, MD,
MBA, FACC, writing committee chair and director of electrophysiology
and program director of the Mercy One North Iowa Cardiovascular
Fellowship, in a statement from ACC. “Although improved monitoring leads
to improved detection of arrhythmia after a stroke, there remains less
clarity on the effect this detection has on secondary stroke
prevention.”
Stroke is a leading cause of disability and death
worldwide and identifying its underlying cause is critical to preventing
recurrent events. AF is a common but often silent arrhythmia, and it
significantly increases stroke risk.
Traditional
methods of AF diagnosis, including brief electrocardiogram (ECG)
recordings, often fall short of capturing transient AF, so longer
duration of monitoring can increase the rate of AF detection, was one of
the key takeaways from list created by Geoffrey D. Barnes, MD,
MSc, FACC, associate professor, Frankel Cardiovascular Center,
University of Michigan. He noted the document also states the longer the
time interval between the ischemic stroke and the detected AF episode
decreases the likelihood of AF as a proximal cause of the prior event.
Barnes
said in his takeaways that various technologies have been developed to
identify AF, including continuous or intermittent ambulatory ECG
monitors, which have gained wide adoption in the past few years. There
are also medical-grade monitors (typically electrical activity
monitoring) and consumer-grade monitors (either electrical activity
monitoring or photoplethysmography) can also help in monitoring these
patients.
Arrhythmia monitoring after a stroke requires three
important steps. First, a multidisciplinary evaluation should be
undertaken to identify potential mechanism for stroke. Second, risk
assessment is performed to determine the likelihood that a cardiac
arrhythmia played a role in the stroke (or future stroke). Third, an
optimal monitoring strategy should be selected to be accurate,
practical, and establish follow-up.
For patients in whom
arrhythmia monitoring detects >5 minutes of AF, anticoagulation is
likely recommended. This is particularly true if their CHA2DS2-VASc
score is ≥3. For those with no AF, continuing antiplatelet therapy is
recommended, Barnes wrote.
Does your doctor have enough competence to get this research done in humans? NO? So, you DON'T have a functioning stroke doctor, do you?
With your chances of getting dementia post stroke, your competent?
doctor needs to be monitoring this and provide dementia prevention
solutions. Over a decade to accomplish that! Was it done? NO? So, you DON'T have a functioning stroke doctor, do you? YOUR DOCTOR IS RESPONSIBLE FOR PREVENTING THIS!
Stress
signals in the brain's clean-up cells may be linked to nerve
degeneration in Alzheimer's disease, leading to memory loss and other
symptoms.
Blocking
the integrated stress response pathway in mouse brains prevented damage
to synapse connections and reduced the buildup of toxic tau proteins
associated with Alzheimer's.
Researchers
from CUNY have identified a novel neurodegenerative microglia phenotype
in Alzheimer's disease, characterized by a stress-related signaling
pathway that causes brain immune cells to become harmful.
See a mistake?
A
sequence of stress signals among specialized clean-up cells in the
brain could at last reveal why some immune responses can cause
significant nerve degeneration that results in the loss of memory,
judgement, and awareness behind Alzheimer's disease.
Blocking
this pathway in mouse brains modeled on Alzheimer's prevented damage to
their synapse connections and reduced the buildup of potentially toxic tau proteins – both hallmarks of the condition.
The
researchers, led by a team from the City University of New York (CUNY),
believe this pathway – called the integrated stress response (ISR) –
causes brain immune cells called microglia to go 'dark' and start damaging rather than benefiting the brain.
The researchers looked at the effects of stress on microglia cells. (Flury et al., Neuron, 2024)
"We set out to answer what are the harmful microglia in Alzheimer's disease and how can we therapeutically target them," says CUNY neuroscientist Pinar Ayata.
"We
pinpointed a novel neurodegenerative microglia phenotype in Alzheimer's
disease characterized by a stress-related signaling pathway."
Haywire immune cells have previously been linked to Alzheimer's, prompting the team to use an electron scanning process to identify the buildup of dark microglia in human brains affected by Alzheimer's.
Finding
around twice as many stressed microglia in brains with the condition
compared with healthy brains, the researchers went on to show how the
ISR pathway was causing dark microglia to release harmful lipids into
the brain's tissues.
It was these damaging fats that caused the damage to synapses and neuron communication seen in Alzheimer's.
Brain scans were used to identify dark microglia. (Flury et al., Neuron, 2024)
As
is often the case with Alzheimer's research, a better understanding of
how the disease operates can also give scientists more ideas for how to treat it.
If treatments that block ISR can work safely and effectively in humans,
the method could potentially slow the chaos that Alzheimer's causes in
our own brain.
"These findings reveal a critical link between cellular stress and the neurotoxic effects of microglia in Alzheimer's disease," says molecular biologist Anna Flury from CUNY."Targeting
this pathway may open up new avenues for treatment by either halting
the toxic lipid production or preventing the activation of harmful
microglial phenotypes."
The team behind this study found that the misfolded protein malfunctions
that often drive dementia could be triggering the ISR to begin with,
meaning that these signals are both a result of Alzheimer's and a reason
for its further progression.
Further
studies should make this relationship clearer, now that we have a
better idea of how the ISR pathway and dark microglia act in the brain –
and from there, hopefully, new approaches to therapies.
It is your competent? doctors' complete responsibility to prevent post stroke depression by having EXACT 100% RECOVERY PROTOCOLS! No protocols, you DON'T have a functioning stroke doctor! Don't know what s/he is but without protocols, they are useless!
Send
me hate mail on this: oc1dean@gmail.com. I'll print your complete
statement with your name and my response in my blog. Or are you afraid
to engage with my stroke-addled mind? I would like to know why you
aren't solving stroke to 100% recovery, and what is your definition of
competence in stroke? Swearing at me is allowed, I'll return the favor.
Question
Does the association between depression and dementia persist whether depression is diagnosed in early, middle, or late life?
Findings
In this population cohort study of more than 1.4 million adult
Danish citizens followed up from 1977 to 2018, the risk of dementia
more than doubled for both men and women with diagnosed depression and
was higher for men than women; the risk of dementia persisted whether
depression was diagnosed in early, middle, or late life.
Meaning
Dementia risk associated with depression diagnosis was higher
for men than women; the persistent association between dementia and
depression diagnosed in early and middle life suggests that depression
may increase dementia risk.
Abstract
Importance
Late-life depressive symptoms are associated with subsequent
dementia diagnosis and may be an early symptom or response to
preclinical disease. Evaluating associations with early- and middle-life
depression will help clarify whether depression influences dementia
risk.
Objective
To examine associations of early-, middle-, and late-life depression with incident dementia.
Design, Setting, and Participants
This was a nationwide, population-based, cohort study
conducted from April 2020 to March 2023. Participants included Danish
citizens from the general population with depression diagnoses who were
matched by sex and birth year to individuals with no depression
diagnosis. Participants were followed up from 1977 to 2018. Excluded
from analyses were individuals followed for less than 1 year, those
younger than 18 years, or those with baseline dementia.
Exposure
Depression was defined using diagnostic codes from the International Classification of Diseases (ICD) within the Danish National Patient Registry (DNPR) and Danish Psychiatric Central Research Register (DPCRR).
Main Outcomes and Measure
Incident dementia was defined using ICD diagnostic
codes within the DPCRR and DNPR. Cox proportional hazards regression was
used to examine associations between depression and dementia adjusting
for education, income, cardiovascular disease, chronic obstructive
pulmonary disease, diabetes, anxiety disorders, stress disorders,
substance use disorders, and bipolar disorder. Analyses were stratified
by age at depression diagnosis, years since index date, and sex.
Results
There were 246 499 individuals (median [IQR] age, 50.8
[34.7-70.7] years; 159 421 women [64.7%]) with diagnosed depression and
1 190 302 individuals (median [IQR] age, 50.4 [34.6-70.0] years; 768 876
women [64.6%]) without depression. Approximately two-thirds of those
diagnosed with depression were diagnosed before the age of 60 years
(684 974 [67.7%]). The hazard of dementia among those diagnosed with
depression was 2.41 times that of the comparison cohort (95% CI,
2.35-2.47). This association persisted when the time elapsed from the
index date was longer than 20 to 39 years (hazard ratio [HR], 1.79; 95%
CI, 1.58-2.04) and among those diagnosed with depression in early,
middle, or late life (18-44 years: HR, 3.08; 95% CI, 2.64-3.58; 45-59
years: HR, 2.95; 95% CI, 2.75-3.17; ≥60 years: HR, 2.31; 95% CI,
2.25-2.38). The overall HR was greater for men (HR, 2.98; 95% CI,
2.84-3.12) than for women (HR, 2.21; 95% CI, 2.15-2.27).
Conclusions and Relevance
Results suggest that the risk of dementia was more than
doubled for both men and women with diagnosed depression. The persistent
association between dementia and depression diagnosed in early and
middle life suggests that depression may increase dementia risk.
