Use the labels in the right column to find what you want. Or you can go thru them one by one, there are only 29,286 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.
This is the whole problem in stroke enumerated in one word; 'care' NOT RECOVERY!
YOU have to get involved and chance this failure mindset of 'care' to 100% RECOVERY!
I wouldn't go there for stroke; they refer to 'care; NOT RECOVERY! Survivors want 100% recovery; this center does nothing of the sort! YOU are going to have to scream at them for not showing these three results:
There is no quality here if you don't measure the right things.
You'll want to know results so call that hospital president(whomever that is) RESULTS
are; tPA efficacy, 30 day deaths, 100% recovery. Because there is no
point in going to that hospital if they are not willing to publish
results.
HOUSTON, TX -- St. Luke’s Health-The Vintage Hospital has received certification from DNV as a Primary Stroke Center and designation as a Primary (Level III) Stroke Facility from the Texas Department of State Health Services (DSHS). These achievements affirm the hospital’s readiness to handle a full range of stroke-related medical problems.
“These
recognitions let our community know that our hospital has the
combination of the necessary equipment, expert staff and extensive
training to provide the best possible stroke care," said Mario Garner,
president of St. Luke’s-The Vintage. “Achieving certification from DNV
and designation from DSHS validates the effort our teams have put into
this program to ensure the health of our patients.”
The
DNV Primary Stroke Center Certification is based on standards set forth
by the Brain Attack Coalition and the American Stroke Association, and
affirms that a hospital addresses the full spectrum of stroke care –
diagnosis, treatment, rehabilitation and education – and establishes
clear metrics to evaluate outcomes.
Hospitals
designated as a Primary (Level III) Stroke Facility must meet the
DSHS-approved national stroke standards of care for a Primary Stroke
Center, participate in the hospital's Regional Advisory Council and
regional stroke plan, and submit data to the department as requested.
According
to the American Stroke Association, stroke is a leading cause of death,
killing nearly 130,000 people each year, and is a leading cause of
serious, long-term adult disability. Because stroke or “brain attack”
affects blood flow to the brain, rapid and effective treatment can save
lives and provide the best chance of limiting the extent of long-term
damage.
The increasing number of strokes and subsequent rehabilitation has
highlighted the growing need for effective care(NOT RECOVERY!) strategies. Serious side
effects, such as motor paralysis, can be challenging to mend, but the
recent incorporation of robots into treatment has shown promise.
Automated robots repeatedly provide the proper movements necessary to
recover motor function. However, to ensure appropriate care(NOT RECOVERY!) tailored to
the degree of motor paralysis, knowledge of robots and rehabilitation
is needed.
Osaka Metropolitan University Professor Takashi Takebayashi of the
Graduate School of Rehabilitation Science led a team in collecting data
from the actual use of Teijin Pharma Ltd.'s rehabilitation robot
ReoGo-J.
The team looked into the rehabilitation programs that were selected
by medical staff to match the degree of motor paralysis. By analyzing
the data, the group developed the world's first system that
automatically recommends the optimal rehabilitation program. Based on a
simple test to check the degree of motor paralysis in a patient's hands,
an appropriate treatment can be determined.
By using this system, as long as medical professionals can carry out
the test, even staff without experience with robots can provide
appropriate robotic rehabilitation for motor paralysis. We hope this
will lead to the further promotion of robot rehabilitation and a
reduction in the burden on medical staff."
Professor Takashi Takebayashi, Graduate School of Rehabilitation Science, Osaka Metropolitan University
1Department
of Rehabilitation Medicine, Xishan People’s Hospital of Wuxi City, Wuxi
Branch of Zhongda Hospital Southeast University, Wuxi, People’s
Republic of China; 2Department of Orthopedics, The 904th
Hospital of the Joint Logistics Support Force of the PLA, Wuxi, Jiangsu,
People’s Republic of China; 3Department of Orthopedics, The Army 947th Hospital, Kashgar, People’s Republic of China; 4Department
of Neurosurgery, Xishan People’s Hospital of Wuxi City, Wuxi Branch of
Zhongda Hospital Southeast University, Wuxi, People’s Republic of China
*These authors contributed equally to this work
Correspondence:
Yelei Zhang, Department of Neurosurgery, Xishan People’s Hospital of
Wuxi City, Wuxi Branch of Zhongda Hospital Southeast University, Wuxi,
People’s Republic of China, Email Zhangyelei2019@163.com
Abstract:
Patients with stroke would have persistent functional deficits despite
undergoing physiotherapy and rehabilitation training. Recently(WRONG! Since July 2012! and you DIDN'T KNOW THAT? My God, you're incompetent!), vagus
nerve stimulation (VNS), a newly emerging neuroregulatory technique, has
been shown to improve motor dysfunction after stroke. Evidence from
clinical and preclinical studies has proven the safety, feasibility, and
efficacy of invasive and noninvasive VNS. It has been reported that the
positive effect may be related to anti-inflammatory effects, mediating
neuroplasticity, increasing blood–brain barrier integrity, promoting
angiogenesis and reducing spreading depolarization. However, the
underlying mechanism remains poorly understood. In this review, we have
summarized the potential molecular mechanisms by which VNS promotes
stroke prognosis. We believe(It's already been proven for over a decade!) that VNS combined with upper-extremity
rehabilitation can improve impairment and function among moderately to
severely impaired stroke survivors. The applications and further
exploration are discussed to provide new insights into this novel
therapeutic technique.
Stroke is the leading cause of long-term disability worldwide, with
80% of patients suffering from motor dysfunction on one side of the
body, which seriously affects their quality of life.1
According to the pathophysiology, stroke could be identified into two
principal categories: ischemic and hemorrhagic stroke. Ischemic stroke
occurred when blood flow is insufficient and unable to satisfy the brain
tissue’s needs for oxygen and nutrients. In contrast, hemorrhagic
stroke is due to the rupture of a blood vessel and represented by blood
in the cerebral parenchyma, which can accumulate and press on the
adjacent parenchyma.2
Similarly, both ischemic and hemorrhagic stroke would be associated
with neurological dysfunction. Despite receiving physiotherapy and
rehabilitation training, many patients still have persistent functional
deficits, which would limit the quality of their lives and carry a huge
economic burden on families and society.3
Therefore, novel therapeutic strategies are needed to better promote
the improvement of damaged neurological function following stroke.
Vagus nerve stimulation (VNS) is a newly emerged neuroregulatory
technique in recent years that has been widely used for the treatment of
multiple neurological diseases such as refractory epilepsy, migraines,
and refractory depression. An increasing number of studies have shown
that VNS combined with rehabilitation can significantly reduce the size
of post-stroke cerebral infarctions, reduce neurological symptoms, and
improve limb motor function following stroke.4
VNS is commonly classified as invasive VNS (iVNS) or noninvasive VNS
(nVNS). The nVNS containing auricular VNS in the ear (ta-VNS) and
cervical VNS in the neck (tc-VNS) exhibited central nervous system (CNS)
activation, similar to invasive VNS. However, the role of VNS in
post-stroke motor function has not yet been elucidated and the
mechanisms remain unclear. Given that the vagus nerve (VN) plays pivotal
roles in the CNS regulating inflammatory responses and emerging
evidence link inflammatory processes with VNS, the anti-inflammatory
potential of VNS has been discovered.5
VNS has also been demonstrated to ameliorate gut microbiota dysbiosis
and modulate microbiota-gut-brain axis to promote functional recovery
after stroke.6,7
In this study, we summarized the anatomical, pre-clinical, and clinical
evidence of VNS. We further emphasized the possible mechanism of VNS in
improving motor dysfunction after stroke based current evidence and
analyzed future challenges for its clinical application.
What good does this do to get survivors recovered? That's the whole point of stroke research! If you can't explain that you don't belong in stroke!
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.
And you don't know about much faster ways to determine infarct or bleed?
A
simplified patient selection paradigm with noncontrast computed
tomography (NCCT) can reduce the time to reperfusion and widen the
eligibility of acute ischemic stroke large vessel occlusions (LVOs) for
endovascular therapy. The objectives of this article are (1) to develop,
train, and internally validate a deep learning algorithm that estimates
baseline infarct core volume (ICV) on NCCT in anterior circulation LVO
patients, and (2) by using an external set, to ascertain how this
algorithm's (aICV‐NCCT) predictive performance compares with Alberta
Stroke Program Early Computed Tomography Score‐NCCT and ICV‐CT perfusion
in its capacity to estimate the final infarct volume established on
diffusion‐weighted magnetic resonance imaging at 24‐ to 48‐hour
follow‐up.
METHODS
In
the first phase, stroke activations with baseline NCCT and CT
angiography were used to train an aICV‐NCCT. The algorithm was then
internally validated using intraclass correlations and Intersection over
Union. In the external set, patients with LVO treated with endovascular
therapy achieving modified Thrombolysis in Cerebral Infarction score
≥2b and available baseline NCCT, CT angiography, and CT perfusion were
included.
RESULTS
A
total of 2858 studies of patients with stroke alerts were used for
training (80%) and internal validation (20%). We obtained a high
correlation (intraclass correlation coefficient, 0.78; CI, 0.73–0.83)
and an acceptable Intersection over Union of 0.24 on the internal
validation set. The external set consisted on 230 patients with an LVO.
When predicting final infarct volume on the external set, our aICV‐NCCT
was similar to ICV‐CT perfusion (intraclass correlation coefficient,
0.50 versus 0.54; P = 0.764) and Alberta Stroke Program Early Computed Tomography Score‐NCCT (rs, −0.41; P = 0.436).
CONCLUSION
In
this study, we developed and validated a deep learning algorithm that
demonstrates an at least equivalent performance to CT perfusion in
estimating core volume on acute stroke imaging studies in patients with
suspected anterior circulation LVO strokes. The algorithm's robust
performance holds significant potential in settings with limited access
to advanced imaging technologies across diverse healthcare environments.
Ask your competent? doctor how this will be used in your favor to slow down brain aging. NO knowledge; you DON'T have a functioning stroke doctor! RUN AWAY!
Summary: A study reveals how brain cell interactions
influence aging, showing that rare cell types either accelerate or slow
brain aging. Neural stem cells provide a rejuvenating effect on
neighboring cells, while T cells drive aging through inflammation.
Researchers used advanced AI tools and a spatial single-cell atlas to
map cellular interactions across the lifespan in mice.
This work
sheds light on how interventions, such as enhancing neural stem cells,
might combat neurodegeneration. By understanding these cellular
dynamics, scientists can explore tailored therapies to slow aging and
promote brain resilience. The findings also offer insights into
conditions like Alzheimer’s disease, highlighting the importance of
cell-to-cell interactions.
Key Facts:
Rejuvenating Role: Neural stem cells create a supportive environment that rejuvenates nearby cells, even outside their lineage.
Aging Impact: T cells accelerate brain aging through pro-inflammatory signals, especially interferon-γ.
Innovative Tools: Researchers used a spatial transcriptomic atlas and machine learning models to study brain aging at the cellular level.
Source: Stanford
Much
like plants in a thriving forest, certain cells in the brain create a
nurturing environment, enhancing the health and resilience of their
neighbors, while others promote stress and damage, akin to a noxious
weed in an ecosystem.
A new study published in Nature on
December 18, 2024, reveals these interactions playing out across the
lifespan. It suggests local cellular interactions may profoundly
influence brain aging — and offers fresh insights into how we might slow
or even reverse the process.
“What was exciting to us was finding
that some cells have a pro-aging effect on neighboring cells while
others appear to have a rejuvenating effect on their neighbors,”
said Anne Brunet, the Michele and Timothy Barakett Endowed Professor in
Stanford’s Department of Genetics and co–senior investigator of the new
study.
These
findings are important, says Zou, “because they highlight how cellular
interactions — not just the intrinsic properties of individual cells —
shape the aging process.” Credit: Neuroscience News
Specifically,
Brunet said, “We were surprised to discover that neural stem cells,
which we’ve studied for a long, long time, had a rejuvenating effect on
the cells around them. In the future we want to understand the role of
neural stem cells in providing a beneficial environment for resilience
within the brain.”
Brunet collaborated with James Zou, an
associate professor of biomedical data science at Stanford, to conduct
the study, which was spearheaded by graduate student, Eric Sun.
Brunet’s
lab, a leader in brain aging and neural stem cell biology, provided the
biological expertise and experimental framework. Zou’s team brought
cutting-edge AI techniques to analyze the data, while Sun, with a
background in physics and quantitative analysis, acted as the bridge
between these two worlds.
The research was supported by a Catalyst
Award from the Knight Initiative for Brain Resilience at Stanford’s Wu
Tsai Neurosciences Institute.
These findings open new avenues of
research, including examining how rejuvenating interventions like
exercise and reprogramming factors promote brain health, potentially by
enhancing the brain’s natural resilience and repair mechanisms. Such
insights may suggest new strategies to combat neurodegeneration and
cognitive decline.
The findings may also help scientists
understand how diseases such as Alzheimer’s disease change the way cells
interact and drive brain aging.
Cells that age — and rejuvenate — the brain
The
research team set out to tackle a fundamental question: How do cells in
their native environment influence one another during the aging
process?
Previous studies have focused on individual cells in
isolation, overlooking the critical context of their “neighborhoods”
— the cells surrounding them.
By preserving and analyzing these
spatial relationships, the team aimed to uncover whether interactions
between different cell types either drive or mitigate aging in the
brain.
Their investigation revealed a striking finding: Out of the
18 different cell types the researchers identified, two rare cell types
had powerful but opposing effects on nearby cells.
T cells,
immune cells that infiltrate the aging brain, have a distinctly
pro-inflammatory, pro-aging effect on neighboring cells that may be
driven by interferon-γ, a signaling molecule that drives inflammation.
On
the other hand, they found that neural stem cells, though rare,
demonstrate a powerful rejuvenating effect, even on nearby cells outside
the neural lineage.
During brain development, neural stem cells
mature into the major cell types in the brain; in adults, they can also
give rise to new neurons and are important for maintenance and repair of
the nervous system.
Beyond their well-established ability to
generate healthy new neurons, the new study suggests NSCs may help
create a supportive environment for brain cells.
These findings
are important, says Zou, “because they highlight how cellular
interactions — not just the intrinsic properties of individual cells
— shape the aging process.”
Building a map and models
At
the heart of this research are three key innovations by the research
team: a spatial single-cell atlas of gene activity in the mouse brain
across its lifespan and two advanced computational tools, each essential
for piecing together how cells influence one another as they age.
To
map the complex neighborhoods of the brain, the researchers created a
spatial single-cell transcriptomic atlas of the mouse brain, capturing
gene expression data from 2.3 million cells across 20 stages of life,
equivalent to human ages 20 to 95.
Unlike traditional methods that
separate complex tissues, like the brain, into a collection of many
disconnected cells, this experimental approach preserved the spatial
relationships between cells, allowing the team to study how their
spatial proximity shapes aging.
The atlas laid the groundwork for
the first computational tool — a spatial aging clock. The clocks are
machine-learning models designed to predict the biological age of
individual cells based on their gene expression.
“For the first
time, we can use aging clocks as a tool to discover new biology,” says
Sun, instead of just using them to estimate biological age.
The
second tool, built using graph neural networks, provided a powerful way
to model these cell-to-cell interactions. By creating a kind of in
silico brain, the researchers could simulate what happens when specific
cell types are added, removed, or altered. This allowed them to explore
potential interventions that would be nearly impossible to test in a
living brain.
“This computational tool allows us to simulate what
happens when we perturb individuals cell in the brain, which is
something we can’t really test experimentally at scale,” says Zou.
To
ensure the broader scientific community can build on their findings,
Sun has made their tools and code publicly available, providing a
valuable resource for studying cellular interactions across various
tissues and organisms.
Implications and future directions
The
study offers major insights into the drivers of aging, as well as
rejuvenating factors that could help restore resilience and vitality to
the aging brain.
“Different cells respond differently to rejuvenating interventions,” explains Brunet.
“Brain
aging is exceptionally complex, so future therapies will need to be
tailored not only to tissues but also to the specific cell types within
those tissues.”
By demonstrating how spatial context and proximity
influence cellular aging, the research builds on longstanding theories
about the role of immune and senescent cells in the aging process.
Looking ahead, the team hopes to move from observation to causation.
“If
we prevent T cells from releasing their pro-aging factors or enhance
the effects of neural stem cells, how does that change the tissue over
time?” asks Brunet.
While the study focused on mice, the team also
hopes to extend their approach to human tissues. “We’re working to make
these tools broadly applicable to other tissues and biological
processes,” adds Sun.
Funding
The research
was supported by the the Knight Initiative for Brain Resilience at
Stanford’s Wu Tsai Neurosciences Institute, the Stanford Knight-Hennessy
Scholars Program, the National Institutes of Health (P01AG036695,
R01AG071711), a National Science Foundation (Graduate Research
Fellowship, CAREER award 1942926), P.D. Soros Fellowship for New
Americans, Silicon Valley Foundation, Chan Zuckerberg Biohub–San
Francisco Investigator program, Chan Zuckerberg Initiative, the Milky
Way Research Foundation, the Simons Foundation, and a generous gift from
M. and T. Barakett.
Competing Interests
Brunet is a scientific advisory board member of Calico.
About this genetics and neuroscience research news
Author: Nicholas Weiler Source: Stanford Contact: Nicholas Weiler – Stanford Image: The image is credited to Neuroscience News
I don't yet have mittens that can be cinched at the wrist since otherwise with no use of the hand there is no way the mitten stays on. So today when walking in my nearby woods at 30 degrees with a north wind blowing my exposed left hand was getting cold. That shouldn't be a problem, I just put it in my left jacket pocket. Not so, the left hand has no ability to even remotely get close to the pocket on its' own, so I have to try to get it in with my right hand, probably failed 6 times with my pinkie finger catching the zipper. After spending 15-20 minutes i finally got it inserted into the pocket.
This is the whole problem with spasticity; TREATING, NOT CURING! Don't we have anyone in stroke smart enough to cure spasticity? Instead we get the infuriating opinion of Dr. William M. Landau that seems to have short-circuited spasticity research. Schadenfreude can't come soon enough for him.
XEOMIN® (incobotulinumtoxinA) got approval from Health Canada for
treating spasticity in adults in the post-stroke lower limb. A
significant step in healthcare history for Canada, this is yet another
vital milestone in the wider application for XEOMIN, through which
healthcare providers can eventually treat upper and lower limb
spasticity in the same patient by combining the two limbs into a total
of 600 units. With this label expansion for XEOMIN, its basal role is
now underpinned as a fundamental tool in neurological rehabilitation
improvement(NOT GOOD ENOUGH! Survivors want 100% recovery! GET THERE!) of ambulation to a reduction in pain. Every year, more than
109,000 strokes adversely affect Canadians. Of this number, a greater
percentage of survivors become spastic one year after their stroke. This
would be the sixth therapeutic use added to XEOMIN in Canada after
others such as cervical dystonia, upper limb spasticity, and chronic
sialorrhea.
But I see no comparison to ecstacy! So, your doctor needs to get further research initiated to determine the best treatment. This is why survivors need this PTSD treatment; your 23% chance of stroke survivors getting PTSD?
A drug that
combines the atypical antipsychotic brexpiprazole and the selective
serotonin reuptake inhibitor sertraline provides significantly greater
relief of posttraumatic stress disorder (PTSD) symptoms than sertraline
plus placebo, results of a phase 3 trial showed.
The medication is
currently under review by the US Food and Drug Administration (FDA) and
if approved, will be the first pharmacologic option for PTSD in more
than 20 years.
The trial met its primary endpoint of change in the
Clinician Administered PTSD Scale for Diagnostic and Statistical Manual
of Mental Disorders-5 (DSM-5) (CAPS-5) total score at week 10 and
secondary patient-reported outcomes of PTSD symptoms, anxiety, and
depression.
“And
what is really cool, what’s really impactful is the combination worked
better than sertraline plus placebo on a brief inventory of psychosocial
functioning,” study investigator Lori L. Davis, a senior research
psychiatrist, Birmingham Veterans Affairs Health Care System,
Birmingham, Alabama, told Medscape Medical News.
“We can
treat symptoms but that’s where the rubber meets the road, in terms of
are they functioning better,” added Davis, who is also an adjunct
professor of psychiatry, Heersink School of Medicine, The University of
Alabama at Birmingham.
The findings were published online on December 18 in JAMA Psychiatry and reported earlier
this year as part of a trio of trials conducted by Otsuka
Pharmaceutical and Lundbeck Pharmaceuticals, codevelopers of the drug.
Clinically Meaningful
The
FDA accepted the companies’ supplemental new drug application in June
with a decision on approval expected in early February 2025.
“This
study provides promising results for a medication that may be an
important new option for PTSD,” John Krystal, MD, director, Clinical
Neuroscience Division, National Center for PTSD, US Department of
Veterans Affairs, who was not involved in the research, told Medscape Medical News. “New PTSD treatments are a high priority.”
Currently, there are two FDA-approved medication treatments for PTSD — sertraline and paroxetine.
“They
are helpful for many people, but patients are often left with residual
symptoms or tolerability issues,” noted Krystal, who is also professor
and chair of psychiatry, Yale University, New Haven, Connecticut.
“New
medications that might address the important ‘effectiveness gap’ in
PTSD could help to reduce the remaining distress, disability, and
suicide risk associated with PTSD.”
The double-blind, phase 3 trial
included 416 adults aged 18-65 years with a DSM-5 diagnosis of PTSD and
symptoms for at least 6 months prior to screening. Patients underwent a
1-week placebo-run in period followed by randomization to daily oral
brexpiprazole 2-3 mg plus sertraline 150 mg or daily sertraline 150 mg
plus placebo for 11 weeks.
Participants’ mean age was 37.4 years,
74.5% were women, and mean CAPS-5 total score was 38.4, suggesting
moderate to high severity PTSD, Davis said. The average time from the
index traumatic event was 4 years and three fourths had no prior
exposure to PTSD prescription medications.
At week 10, the mean
change in CAPS-5 score from randomization was −19.2 points in the
brexpiprazole plus sertraline group and −13.6 points in the sertraline
plus placebo group (95% CI, −8.79 to −2.38; P < .001).
Asked
whether the 5.59-point treatment difference is clinically meaningful,
Davis said there is no widely agreed definition for change in CAPS-5
total score but that a within-group reduction of more than 10-13 points
is most-often cited as being clinically meaningful.
The key
secondary endpoint of least square mean change in the patient-reported
Brief Inventory of Psychosocial Function total score from baseline to
week 12 was −33.8 with the combination vs −21.8 with sertraline plus
placebo (95% CI, −19.4 to −4.62; P = .002).
“That’s
clinically meaningful for me as a provider and a clinician and a
researcher when you’re getting the PTSD symptom change differences in
parallel with the improvement in functional outcome,” she said. “I see
that as the clinically meaningful gauge.”
In terms of safety, 3.9%
of the participants in the brexpiprazole/sertraline group and 10.2% of
those in the sertraline/placebo group discontinued treatment due to
adverse events.
In
both the combination and control groups, the only treatment-emergent
adverse event with an incidence of more than 10% was nausea (12.2% vs
11.7%, respectively).
At the last visit, the mean change in body
weight from baseline was an increase of 1.3 kg for brexpiprazole plus
sertraline vs 0 kg for sertraline alone. Rates of fatigue (6.8% vs 4.1%)
and somnolence (5.4% vs 2.6%) were also higher with brexpiprazole plus
sertraline.
A Trio of Clinical Trials
The findings are part of a larger program reported by the drug makers that includes a flexible-dose brexpiprazole phase 2 trial that met the same CAPS-5 primary endpoint and a second phase 3 trial (072 study) that did not.
“We’ve
looked at that data and the sertraline/placebo response was a lot
higher, so it was not due to a lack of response with the combination but
due to a more robust response with the active control,” Davis said.
“But we want to point out for that 072 study, there was still important
separation between the combination and sertraline plus placebo on the
functional outcome.”
All three trials ran for 12 weeks, so
longer-term efficacy and safety data are needed, she said. Other
limitations of the published phase 3 study are the patient eligibility
criteria, restrictions on concomitant therapy, and lack of non-US sites,
which many limit generalizability, the authors note.
“Specifically,
the exclusion of patients with a current major depressive episode is
both a strength (to show a specific effect on PTSD) and a limitation
(given the high prevalence of comorbid depression in PTSD),” they added.
Kudos, Caveats
Reached
for comment, Vincent F. Capaldi, II, MD, ScM, professor and chair,
department of psychiatry, Uniformed Services University of the Health
Sciences School of Medicine, Bethesda, Maryland, said the exclusion of
these patients is a limitation but that the study was well designed and
conducted in a large sample across the United States.
“The findings suggest that brexpiprazole plus sertraline is a more effective treatment for PTSD than sertraline alone,” he told Medscape Medical News. “This finding is significant for our service members, who suffer from PTSD at higher rates than the general population.”
Additionally,
the significant improvement in psychosocial functioning at week 12 “is
important because PTSD is known to cause significant social and
occupational disability, as well as quality-of-life issues,” he said.
Capaldi
pointed out, however, that the study was conducted only at US sites and
did not specifically target military/veteran persons, which may limit
applicability to these unique populations.
“While subgroup
analyses were generally consistent with the primary analysis, the study
was not powered to detect differences between subgroups,” he added.
“These subgroup analyses are quite important when considering military
and veteran populations.”
Further research is needed to explore
whether certain traumas are more responsive to combination treatment,
the efficacy of augmenting existing sertraline therapy, and the specific
mechanisms of brexpiprazole driving the improved outcomes, Capaldi
said.
This
study was funded by Otsuka Pharmaceutical Development &
Commercialization, which was involved in the design, conduct, and data
analysis. Davis reported receiving advisory board fees from Otsuka and
Boehringer Ingelheim; lecture fees from Clinical Care Options; and
grants from Alkermes, the Veterans Affairs, Patient-Centered Outcomes
Research Institute, Department of Defense, and Social Finance. Several
co-authors are employees of Otsuka.
Krystal reported
serving as a consultant for Otsuka America Pharmaceutical, Aptinyx,
Biogen, IDEC, Bionomics Ltd, Boehringer Ingelheim International,
Clearmind Medicine, Cybin IRL, Enveric Biosciences, Epiodyne, EpiVario,
Janssen, Jazz Pharmaceuticals, Perception Neuroscience, Praxis Precision
Medicines, Springcare, and Sunovion Pharmaceuticals. Krystal also
reported serving as a scientific advisory board member for several
companies and holding several patents.
How incompetent is your hospital in not creating a protocol on this in the past 19 years? Will anyone be fired? I'd suggest firing the board of directors for not setting proper goals for the hospital. Clean everything out from the top and on down.
Background:
3-Hydroxy-3-methylglutaryl-coenzyme A reductase inhibitors (statins),
the most frequently used lipid-lowering agents (LLAs) have
neuroprotective effects in rodent models of ischemic stroke. The authors
hypothesized that patients with ischemic stroke taking LLAs would have
better outcomes than patients not taking LLAs.
Methods:
The Northern Manhattan Study is a population-based study designed to
determine stroke incidence and prognosis in a multiethnic, urban
population. Northern Manhattan residents age 40 years or older diagnosed
with their first ischemic stroke were eligible. Patients or their
proxies were interviewed regarding medications being taken at home
before stroke onset. The NIH Stroke Scale was used to assess stroke
severity, categorized as mild (≤5), moderate (6 to 13), or severe (≥14),
and the Barthel Index at 6 months to assess functional outcome.
Clinical worsening in hospital was recorded by trial neurologists. Odds
ratios and 95% CIs for association of LLA use and stroke severity,
mortality, and functional outcome were calculated using logistic
regression.
Results: Of 650 patients,
57 (8.8%) were taking LLAs. The majority (90.9%) of LLA users were
taking a statin. Clinical worsening in hospital occurred less frequently
among patients taking LLAs at stroke onset (6.3% vs 18.2%; p = 0.04). Ninety-day mortality was lower in those taking LLAs (1.8% vs 10.6%, p = 0.03). The proportion of patients with severe stroke among those taking LLAs was not lower (10.7% vs 16.8%, p = 0.39).
Conclusion:
Patients taking lipid-lowering agents (LLAs) at the time of an ischemic
stroke may have lower poststroke mortality and a lower risk of
worsening during hospitalization. Prospective studies are warranted to
determine whether LLAs, and statins in particular, have neuroprotective
properties or other beneficial effects in acute ischemic stroke.
(This statin therapy should already be in your hyperacute protocol immediately post stroke. Is it? Or is your hospital completely incompetent in that also? Along with everything else in stroke they are incompetent at!
The
ultrasound-guided lateral approach for BoNT-A injections into the
subscapularis is a precise and reliable method for reducing pain and
spasticity and improving quality of life in stroke survivors with
hemiplegic shoulder pain.
Cite this article as:
Neto I, Guimaraes M, Ribeiro T, et al. (December 19, 2024) Retrospective
Cohort Study on the Incidence and Management of Hemiplegic Shoulder
Pain in Stroke Inpatients. Cureus 16(12): e76030.
doi:10.7759/cureus.76030
Background: Painful hemiplegic shoulder (PHS) is a prevalent and
challenging complication following a stroke and can significantly impair
a patient's engagement in rehabilitation, leading to poorer functional
outcomes and extended hospital stays. This retrospective cohort study
aims to investigate the incidence, etiology, and management(Survivors don't want it 'managed'; they want it prevented! Solve the correct problem; what survivors want! Not your ideas!) of PHS in
stroke inpatients, focusing on the effectiveness of various therapeutic
interventions.(Whomever
approved this objective needs to be fired. The objective should have
been to create protocols that cure shoulder pain.)
Methods: We conducted a retrospective analysis of subacute stroke
inpatients who developed PHS during rehabilitation at a single center.
Medical records were reviewed to assess the incidence of PHS, underlying
causes, and treatment modalities. Primary outcome measures included the
prevalence of PHS, the distribution of identified etiologies, and
therapeutic outcomes associated with different management strategies.
Results: Our findings revealed a significant prevalence of PHS among
stroke inpatients, consistent with existing literature. The
multifactorial etiology included spasticity, adhesive capsulitis,
glenohumeral subluxation, central post-stroke pain, and complex regional
pain syndrome, with advanced age, low functional scores, motor and
sensory impairments, and comorbidities such as diabetes mellitus
identified as key risk factors. Management strategies ranged from
conservative approaches, such as physical modalities and slings, to
advanced interventions, including intra-articular corticosteroid
injections, botulinum toxin type A applications, nerve blocks, and
radiofrequency neuromodulation. Corticosteroid injections and electrical
stimulation were particularly effective in alleviating pain and
improving functional outcomes. Notably, pulsed radiofrequency modulation
targeting the suprascapular and axillary nerves showed superior
efficacy in enhancing the passive range of motion compared to
conventional nerve blocks, although the effectiveness of botulinum toxin
type A was inconsistent.
Conclusions: This study emphasizes the multifaceted nature of PHS in
stroke inpatients, underlining the importance of individualized and
comprehensive treatment strategies. While several therapeutic
interventions, particularly corticosteroid injections and pulsed
radiofrequency, demonstrated effectiveness, the variability in treatment
outcomes highlights the need for further investigation. Future research
should focus on larger patient cohorts with extended follow-up periods
to better elucidate the progression of PHS and refine management
approaches. Despite limitations, including the retrospective study
design and a short follow-up period, these findings provide valuable
insights into the prevalence, progression, and treatment of PHS in
stroke rehabilitation.
Introduction
Stroke remains a leading cause of mortality and disability, imposing
significant socioeconomic and healthcare burdens on developed countries.
Continuous advancements in treatment options have underscored the
importance of early rehabilitation programs in enhancing functional
independence and improving patient outcomes. However, the rehabilitation
process is often hindered by complications, necessitating a
comprehensive understanding of strategies to address these challenges [1].
One such complication is painful hemiplegic shoulder (PHS), a
condition characterized by shoulder pain following a cerebrovascular
accident. Key risk factors for PHS include reduced motor function, type 2
diabetes mellitus (DM2), and a history of prior shoulder pain [2]. Incidence rates of PHS vary widely, from 9% to 73% in earlier reports [3] to more recent findings of 24-64% in inpatient rehabilitation settings [4]. PHS onset varies from two weeks to three months post-stroke, reflecting the heterogeneity of this condition [5].
This condition significantly impairs patients' participation in
rehabilitation, resulting in lower Barthel scores at discharge, poorer
functional recovery, and extended hospital stays [6].
The multifactorial etiology of PHS includes both musculoskeletal and
neurological changes. Common contributors are spasticity, adhesive
capsulitis, glenohumeral subluxation, central post-stroke pain, and
complex regional pain syndrome [7].
Risk factors such as advanced age, low functional scores, dependence on
transfers, neglect, sensory changes, and comorbidities like diabetes
mellitus or depression further complicate the clinical picture [8].
Managing PHS is a significant clinical challenge, but effective
treatment can enhance patients' participation in rehabilitation, leading
to better functional outcomes. Treatment modalities range from
conservative approaches, such as physical modalities and slings, to
minimally invasive techniques, including intra-articular corticosteroid
injections, botulinum toxin injections, nerve blocks, and radiofrequency
neuromodulation [9].
Study aim
Given the diverse etiological factors and management strategies for
PHS, this retrospective study aimed to determine the prevalence of each
identified cause and evaluate the range of treatment options implemented
in an inpatient rehabilitation setting.
The only reason there is post stroke depression is because your INCOMPETENT DOCTOR has not created 100% recovery protocols!
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?
INDIANAPOLIS (WISH) — 800,000 people in the U.S. will suffer from a stroke this year.
It's the leading cause of long-term disability. It can impact a person's speech, movement and memory.
When
treating patients who have had their life changed by a stroke, there
are limits to what medicine can do.(So, you've given up on solving stroke to 100% recovery! GET THE HELL OUT OF STROKE THEN! And find something easier like basket weaving!) That's why new interventions are
being used that help promote resilience after a stroke.
"I felt like a pulsing all the way in the back of my head," said Quincy Taylor.
That was the moment Taylor's life changed forever.
"It was the worst pain that I've experienced so far in my life," Quincy said.
He
suffered a stroke and like many survivors, he faced months of rehab
working on his balance and coordination. That's not all survivors
struggle with.
"Half
of all stroke survivors will experience post-stroke depression at some
point in time after their stroke," said Dr. Alexandra Terrill, a
clinical psychologist at University of Utah Health.
Post-stroke
depression can impact a patient's motivation for rehab and can lead to
social isolation. Studies show rates of hospitalization increase and
relationships can suffer. Terrill led a study using positive psychology
to help stroke survivors and their caregivers.
"Positive
psychology is really something that's focused on the strengths or
resources that an individual has and that can be built upon," Terrill
said.
The eight-week program
helps couples practice goal setting, communication strategies,
gratitude, finding meaning and fostering connections with each other and
those in their social circles.
"We saw a dramatic increase in resilience for the person who had the stroke," Terrill said.
Resilience
is a person's ability to adapt and cope when faced with the challenges
both mentally and physically after a stroke – and building resilience is
just as important for the caregiver.
"Right now, I'm feeling like I'm doing a little bit better than what I was before," Taylor said.
The
NIH reports that people who suffer post-stroke depression are more
likely to be dependent for life on caregivers and have a higher risk of
having another stroke. Dr. Terrill believes positive psychology can be a
simple, cost-effective and life-saving solution to post-stroke
depression. A larger NIH funded study is being conducted now across the
United States.
This story was created from a script aired on WISH-TV. Health Spotlight is presented by Community Health Network.
I don't think I ever talked to a neurologist ever, I had a PMR doctor who knew nothing about recovery as proven by writing three prescriptions of E.T.(Evaluate and Treat). Here is an opinion of neurologists you won't like:
In this video(at link), M. Elizabeth Ross, MD, PhD, FANA,
president of the American Neurological Association, spoke with Healio
about her favorite takeaway from the ANA Annual Meeting in Orlando.
“We’re transforming from a neurological
specialty, where we make the diagnosis and can’t offer much after that,
to a truly interventional specialty with many tools at our command,”
said Ross, who is also director of the Center for Neurogenetics at Weill
Cornell Medicine.
Stroke
is a leading cause of long-term disability, significantly affecting
patients' motor skills and daily activities. Traditional rehabilitation
methods, while beneficial, often lack the precision and adaptability
required for optimal recovery. This paper explores the integration of
deep learning models optimized with Particle Swarm Optimization (PSO) to
enhance stroke rehabilitation outcomes using brain-computer interface
(BCI) technology. We employed a dataset from the BCI Competition IV,
which includes EEG data from multiple participants engaged in motor
imagery tasks. Various deep learning models, including Convolutional
Neural Networks (CNN), Recurrent Neural Networks (RNN), EEGNet, and
Multi-layer Perceptrons (MLP), were optimized using PSO to improve
classification accuracy. The results demonstrate that PSO significantly
enhances the performance of these models, providing a robust framework
for developing advanced rehabilitation systems. This approach not only
improves the accuracy of motor imagery classification but also offers a
personalized rehabilitation experience for stroke patients,
