Use the labels in the right column to find what you want. Or you can go thru them one by one, there are only 33,991 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.
Showing posts with label hemorrhage cascade of death. Show all posts
Showing posts with label hemorrhage cascade of death. Show all posts
Does the definition of medical malpractice include survivors not getting to 100% recovery because their doctors/hospital have done nothing in decades to get stroke solved? Ask your competent? doctor that question. If survivors were to bill their hospital/doctors for $1,000 a dead neuron after successful reperfusion of an ischemic stroke or successful stoppage of a bleeder, that would instantly trigger massive amounts of stroke research to solve the problem.(My bill would have been 5.4 billion dead neurons; so 5.4 trillion dollars!) The rush to solve the neuronal cascade of death and the hemorhage cascade of death would be instantaneous.
HOFFMAN ESTATES, Ill. (WLS) -- A
suburban family will receive $40 million in a medical malpractice
lawsuit after a man was left permanently disabled by a stroke.
Their attorneys said doctors failed to properly treat Antonio DeAngelo's symptoms and his stroke could have been prevented.
DeAngelo
was once a man standing tall. Now, the Hoffman Estates man is unable to
walk long distances, bathe on his own and speak without assistance.
He now carries around a card that reads, "I have aphasia, a loss for words not intelligence."
His family said it's something he will have to carry for the rest of his life and something that could have been prevented.
"The last nine years of our lives and that of our children have been a living hell," his wife Jennifer DeAngelo said.
The
former full-time landscaper went to a doctor with Advocate Physician
Partners, which is affiliated with Advocate Health, seeking treatment
for a spike in his blood pressure in 2015, according to court records.
Instead of ordering a lab test, blood work or EKG, the doctor sent him
home for flu-like symptoms. His attorney said he did not receive blood
pressure medicine.
"Certainly
would have reduced his blood pressure within what's called goal range
within 30 days, and would have prevented Tony's stroke," family attorney
Brad Cosgrove said.
A few weeks later he suffered a stroke and now is re-learning how to walk.
"No
one could ever understand what it means to go through life with a
husband who one day is working full time to suddenly being completely
disabled and requiring 'round the clock care for the rest of his life,"
Jennifer said. "Every day we cry."
This week, the family received a record-breaking nearly $40 million verdict for a stroke patient in the state of Illinois.
A spokesperson for Advocate Physician Partners issued a statement about the situation.
"Our
hearts go out to this individual," the statement read. "It's important
to note that this individual never received care at our facility and was
treated by a non-employed physician at their private office. Due to
pending litigation, we are unable to comment."
The
family's attorney said DeAngelo's doctor was an independent contractor
of Advocate and is still working in the medical system.
The
family said they hope to start a charity fund to bring awareness to
aphasia as the father of two attempts to get his life back.
"They do look forward to life getting a little bit easier," Jennifer said.
You'll want this solved before you have this type of stroke. So ask your doctor and hospital EXACTLY WHAT RESEARCH THEY ARE INITIATING TO SOLVE THIS. No research, have the board of directors fired.
Intracerebral
hemorrhage (ICH) can be divided into a primary and secondary phase. In
the primary phase, hematoma volume is evaluated and therapies are
focused on reducing hematoma expansion. In the secondary,
neuroprotective phase, complex systemic inflammatory cascades, direct
cellular toxicity, and blood-brain barrier disruption can result in
worsening perihematomal edema that can adversely affect functional
outcome. To date, all major randomized phase 3 trials for ICH have
targeted primary phase hematoma volume and incorporated clot evacuation,
intensive blood pressure control, and hemostasis. Reasons for this lack
of clinical efficacy in the major ICH trials may be due to the lack of
therapeutics involving mitigation of secondary injury and inflexible
trial design that favors unilateral mechanisms in a complex
pathophysiology. Potential pathophysiological targets for attenuating
secondary injury are highlighted in this review and include therapies
increasing calcium, antagonizing microglial activation, maintaining
macrophage M1 versus M2 balance by decreasing M1 signaling, aquaporin
inhibition, NKCCl inhibition, endothelin receptor inhibition, Sur1-TRPM4
inhibition, matrix metalloproteinase inhibition, and
sphingosine-1-phosphate receptor modulation. Future clinical trials in
ICH focusing on secondary phase injury and, potentially implementing
adaptive trial design approaches with multifocal targets, may improve
insight into these mechanisms and provide potential therapies that may
improve survival and functional outcome.
Spontaneous
intracerebral hemorrhage (ICH) is one of the most common causes of
death and disability in the USA, with over 795,000 new strokes every
year of which 10% are ICH (incidence of 24.6 per 100,000 person-years).1,2 However, while the incidence remains steady, ICH boasts the highest mortality with rates ranging between 53% and 59%1,3,4 and the highest comorbidities in patients 50–80 years old.1
The
primary phase in ICH management, calculating initial hematoma volume
and rate of expansion, has been aggressively targeted in large
multicenter trials over the last 15 years (Table 1).5–11
Despite the number of major clinical trials, all of the novel
therapeutic strategies targeting primary mechanisms from these clinical
trials have been unsuccessful in demonstrating improved functional
outcome, suggesting that secondary mechanisms of injury after ICH may
represent a complementary and essential pathophysiological target.
Table 1. Summary of clinical trials targeting primary phase hematoma volume and expansion.
Table 1. Summary of clinical trials targeting primary phase hematoma volume and expansion.
In
this review, we summarize pathophysiological mechanisms critical in
wound repair after ICH and current evidence from important clinical
trials that suggest viable therapeutic targets for attenuating secondary
injury in patients with ICH. We also propose a new paradigm to
establish novel strategies and targets for future ICH therapy clinical
trials that can specifically target secondary mechanisms of injury. The
lack of efficacy in therapies targeting primary mechanisms in ICH,
emphasizes the need for better prospective clinical trials that both
target and provide quick therapies to mitigate secondary mechanisms of
injury.
You came to the wrong conclusion. The hemorrhage cascade of death is probably responsible for the inflammation rather than the exercise. Do you people have any understanding of stroke at all? And your mentors and senior researchers didn't correct that misunderstanding?
Very early exercise has been reported to exacerbate motor dysfunction; however, its mechanism is largely unknown.
Objective
This
study examined the effect of very early exercise on motor recovery and
associated brain damage following intracerebral hemorrhage (ICH) in
rats.
Methods
Collagenase
solution was injected into the left striatum to induce ICH. Rats were
randomly assigned to receive placebo surgery without exercise (SHAM) or
ICH without (ICH) or with very early exercise within 24 hours of surgery
(ICH+VET). We observed sensorimotor behaviors before surgery, and after
surgery preexercise and postexercise. Postexercise brain tissue was
collected 27 hours after surgery to investigate the hematoma area, brain
edema, and Il1b, Tgfb1, and Igf1 mRNA levels in
the striatum and sensorimotor cortex using real-time reverse
transcription polymerase chain reaction. NeuN, PSD95, and GFAP protein
expression was analyzed by Western blotting.
Results
We observed significantly increased skillful sensorimotor impairment in the horizontal ladder test and significantly higher Il1b
mRNA levels in the striatum of the ICH+VET group compared with the ICH
group. NeuN protein expression was significantly reduced in both brain
regions of the ICH+VET group compared with the SHAM group.
Conclusion
Our
results suggest that very early exercise may be associated with an
exacerbation of motor dysfunction because of increased neuronal death
and region-specific changes in inflammatory factors. These results
indicate that implementing exercise within 24 hours after ICH should be
performed with caution.
This is so fucking easy to explain, the hemorrhage cascade of death is occurring and immediate rehab forestalls that cascade. Whereas in ischemic strokes the
Study investigated the relationship between time to initiation of acute
rehabilitation therapy during hospitalization and disability after
intracerebral hemorrhage (ICH), and identified clinical and patient
characteristics that best predict time to initiation of acute
rehabilitation therapy. Data were obtained from 203 adults with ICH
consecutively admitted to a certified comprehensive stroke center.
Disability was assessed with the modified Rankin Scale (mRS), with poor
outcome defined as mRS score = 4-6 (dependence or worse). Time to
initiation of acute rehabilitation therapy was defined as the number of
days between hospital admission and the first consult by any
rehabilitation therapy specialist (e.g., physical therapy, occupational
therapy, speech therapy). The median number of days from hospital
admission to initiation of acute rehabilitation therapy was 3
(range=2-7). Multivariable logistic regression models indicated that
each additional day between admission and initiation of acute
rehabilitation therapy was associated with increased odds of poor
outcome at 30 days (adjusted odds ratio [OR]=1.151) and at 90 days
(adjusted OR=1.107) for patients with ICH. A multivariable linear
regression model used to identify the predictors of time to initiation
of rehabilitation therapy identified heavy drinking (>5 drinks per
day), premorbid mRS<4, presence of pulmonary embolism, and longer
length of stay in the intensive care unit as independent predictors of
later initiation of acute rehabilitation therapy. Findings suggest that
longer time to initiation of acute rehabilitation therapy after ICH may
have persistent effects on post stroke disability. Delays in acute
rehabilitation therapy consults should be minimized and may improve
outcomes after ICH.
Descriptor Terms: ACUTE CARE,
CLIENT CHARACTERISTICS, FUNCTIONAL STATUS, HEALTH CARE, MEDICAL ASPECTS,
PREDICTION, REHABILITATION SERVICES, SERVICE DELIVERY, STROKE.
Citation: Capo-Lugo, Carmen E. , Askew, Robert
L. , Muldoon, Kathryn , Maas, Matthew , Liotta, Eric , Prabhakaran,
Shyam , Naidech, Andrew. (2020). Longer time before acute rehabilitation therapy worsens disability after intracerebral hemorrhage.
Archives of Physical Medicine and Rehabilitation, 101(5), Pgs. 870-876. Retrieved 7/18/2020, from REHABDATA database.
by
Nicole Lou, Staff Writer, MedPage Today
June 9, 2020
Intracerebral hemorrhage (ICH) has become
increasingly common in recent decades, driven by events in older people,
according to an analysis of the Framingham Heart Study.
The incidence of ICH increased steadily from 25 cases per 100,000
person-years in 1948-1986 (period 1) to 73 cases per 100,000
person-years in 2000-2016 (period 3), reported a team led by
Vasileios-Arsenios Lioutas, MD, of Beth Israel Deaconess Medical Center
and Harvard Medical School.
Altogether, people 75 years and older had ICH reach 176 cases per
100,000 person-years in 2000-2016 (up from 88 per 100,000 in 1948-1986)
in the study published online in JAMA Neurology.
Importantly, the incidence trend differed depending on age:
Remained low in the group ages 45-74 years (not exceeding 25 cases per 100,000 person-years over time)
Increased slightly in people ages 75-84 years (from 96 to 113 cases per 100,000 person-years between periods 1 and 3)
Jumped substantially in the group 85 years and older (from 39 to 287 cases per 100,000 person-years between periods 1 and 3)
This increase coincided with increased use of statins and anticoagulant medications, Lioutas and colleagues noted.
"These findings, in conjunction with the expected increase in life
expectancy, suggest that the absolute number of individuals who
experience an ICH event, particularly at an older age, will likely
continue to increase despite improvements in primary and secondary preventive interventions. Such a trend has already been documented in other high-income countries," they concluded.
Adjusted for age, ICH incidence showed an initial increase followed
by a dip between 1987-1999 (51 cases per 100,000 person-years) and
2000-2016 (46 cases per 100,000 person-years), such that it was no
higher during period 3 compared to period 1.
"This
finding was likely associated with improvements in primary and
secondary preventive practices, which is reflected in the
well-documented decrease in the prevalence of risk factors in the
Framingham Heart Study cohort; both hypertension prevalence and BP levels, which are the most important ICH risk factors, decreased steadily," according to Lioutas and team.
Their analysis drew upon 10,333 Framingham participants (originally
enrolled in 1948) and their children. Of this cohort, 129 (55.8% women,
age 77 on average) had an ICH over 68 years. After applying exclusion
criteria, 99 ICH patients were matched 1:4 by age and sex to controls.
Overall, ICH risk was comparable between men and women. Both deep ICH and lobar ICH grew in incidence with advancing age.
Predictors of deep ICH were higher systolic and diastolic blood
pressure and statin medication use. Factors associated with lobar ICH
were higher systolic blood pressure and apolipoprotein E ε4 allele
homozygosity.
The Framingham cohort was nearly all white, the authors cautioned,
limiting the generalizability of the results to other populations.
Another limitation of the study was that the investigators did not have
data on antiplatelet use.
Last Updated June 09, 2020
Nicole Lou is a reporter for MedPage Today, where she covers cardiology news and other developments in medicine. Follow
Disclosures
The study was
supported by grants from the National Institute of Neurological
Disorders and Stroke; the National Institute on Aging; and the National
Heart, Lung, and Blood Institute.
Lioutas disclosed receiving personal fees from Qmetis.
But have you identified EXACTLY why they died? They didn't die from stroke, they died from a type of brain damage. If you don't know where and when you will never solve Hemorrhagic strokes.
Have you worked on solving these hemorrhage cascade of death problems?
— "We've tried surgery, we've tried medications" -- and not much to show for it
by Crystal Phend,Senior Editor, MedPage Today
February 21, 2020
LOS ANGELES -- Improvements over the past decades
in ischemic stroke mortality haven't been mirrored by even a budge in
hemorrhagic stroke prognosis, a population-based study from the
Netherlands showed.
In the Rotterdam Study, ischemic stroke mortality rates dropped
starting around 1998 for a relative 29% reduction from 1991-1998 to
2008-2015 (29 vs 11 per 100 person-years, P<0.01).
Hemorrhagic stroke mortality rates, though, stayed steady (30 vs 25 per 100 person-years, P=0.93), Reem Waziry, MD, PhD, of Harvard T.H. Chan School of Public Health in Boston, reported here at the International Stroke Conference and online in Stroke.
"It
makes sense, given the amazing advances we've had in the treatment of
ischemic stroke with tPA now 25 years old and endovascular therapy now 5
years old," even though most of these therapies have been aimed at
reducing disability rather than mortality, commented Ralph Sacco, MD,
chairman of neurology at the University of Miami and past president of
the American Heart Association.
"We've had many more failures for hemorrhagic stroke," Sacco told MedPage Today.
"We don't have any major breakthroughs. We've tried surgery, we've
tried medications, and we have not been as successful in altering the
course for hemorrhagic stroke."
There have been some positive developments in hemorrhagic stroke recently, with the STICH trial showing improved mortality with early surgical hematoma evacuation but the MISTIE III trial missing significance for a similar approach with minimally invasive surgery plus thrombolysis.
"Although, these interventions show promise in selected samples of
patients in the setting of clinical trials, these advances are not yet
reflected in the setting of the general population," Waziry's group
wrote in the Stroke paper.
The
study assessed time trends in survival after first-ever strokes among
the 14,926 participants in the long-running prospective study of
middle-age and older adults getting follow-up exams every 3 to 4 years.
After excluding those with a past history of stroke or an unspecified
stroke diagnosis during the study period, there were 162 first-ever
hemorrhagic and 988 ischemic strokes recorded from 1991 through 2015.
Limitations included low power for subgroup analyses, exclusion of
unspecified strokes, and a population of mainly elderly stroke
survivors.
Disclosures
The researchers and Sacco disclosed no relevant relationships with industry.
You'll have to ask your doctor what protocol they are using to prevent this problem from the cascade of death. Since they likely have no protocols ask what researchers they are working with to solve this problem. No researcher contact, call the stroke hospital president and ask why incompetency is allowed in their hospital. Delayed cerebral ischemia is too milquetoast a term to suggest immediate critical response needed, the hemorrhage cascade of death should be used since it implies extreme urgency.
Studies
in subarachnoid hemorrhage (SAH) have traditionally focused on delayed
secondary ischemic injury due to vasospasm, but more recently, attention
has turned to early brain injury (EBI) in patients with poor-grade
injury. The predictable and delayed nature of secondary brain injury
makes SAH a unique illness. Large vessel arterial vasospasm occurs in
approximately 70% of patients starting 3 to 5 days after the initial
hemorrhage, peaking at 5 to 10 days, then slowly resolving over the
following week or two.1Delayed cerebral ischemia (DCI),
defined as infarction, neurologic deterioration, or both from large
vessel vasospasm occurs in about 20% of patients with SAH. Interventions
and clinical investigation have long focused on DCI. Large trials have
failed to improve long-term neurologic outcome despite ameliorating
vasospasm.2 This has led to novel concepts of DCI
pathophysiology, including microthrombosis, neuroinflammation, and
cortical spreading depolarization (SD).1
Subarachnoid
hemorrhage (SAH) is a devastating form of stroke. Oxidative stress
contributes to brain injury, but the mechanisms have been poorly
studied. Here, we evaluated the role of 12/15-lipoxygenase (12/15-LOX),
an enzyme known to cause cell death in ischemic stroke, on brain injury
in a mouse model of SAH.
Methods—
C57Bl6 wild-type mice and Alox15
knockout mice were subjected to SAH using a direct blood injection
technique. In SAH wild-type mice, half received the 12/15-LOX inhibitor
ML351 and half received vehicle. Immunohistochemistry, brain edema,
blood-brain barrier leakage and functional outcomes were assessed 1 and 3
days after SAH induction.
Results—
SAH
led to increased 12/15-LOX in macrophages of the brain parenchyma,
adjacent to the subarachnoid blood. Neuronal cell death after SAH was
reduced by ML351 and in Alox15 knockout mice. Similarly, SAH induced brain edema, which was 12/15-LOX dependent. Finally, Alox15 gene knockout and inhibitor treatment in wild-type mice with SAH led to an improved behavioral outcome.
Conclusions—
12/15-LOX
is overexpressed in macrophages after SAH in mice, and inhibition of
the 12/15-LOX pathway decreases brain injury and improves neurological
outcome. This study suggests 12/15-LOX as a novel therapeutic target to
limit brain injury after SAH.
Every single stroke coming into your stroke hospital should have a protocol to follow. There is never a stroke that is too good to treat. You never magically recover from a stroke. Your doctor should never have to make a subjective decision. You have an objective damage diagnosis(The NIH Stroke Scale is not objective so we have a problem right from the start.). What should follow directly from that is a stroke protocol to remove the clot or stop the bleeding and then a protocol to stop the neuronal cascade of death or the hemorrhage cascade of death. This is so fucking simple, why can't it be done? Laziness? Incompetence? Or just don't care? No leadership? No strategy? Not my job?
The authors undertook this multicenter United States-based survey to
explore factors that influence intravenous thrombolysis decisions
patients with minor stroke, who constitute a controversial category of
acute ischemic stroke. One hundred ninety-four physicians were across
the United States with 150 vignettes using a variation of the following 7
factors that were agreed on by an expert panel as most likely to
influence tPA (tissue-type plasminogen activator) administration:
National Institutes of Health Stroke Scale (NIHSS) score(The NIH Stroke Scale is not objective so we have a problem right from the start.), NIHSS area of
deficit with emphasis on 3 levels (visual/language/weakness), baseline
functional status, previous ischemic stroke, previous intracerebral
hemorrhage, recent use of anticoagulation, and temporal pattern of
symptoms in first hour of emergency department care. One hundred
fifty-six physicians returned complete vignettes and were included in
the final analysis, 80% neurologists and 20% emergency department
physicians; nearly 2/3 practiced in academic institutions and
comprehensive stroke centers. On the 2 extremes of the spectrum,
physicians were most likely to treat patients with higher NIHSS, stable
course, and no prior hemorrhage or ischemic stroke and least likely to
consider treatment in those with low NIHSS, preexisting disability, and
recent stroke or hemorrhage. Overall, 4 of the 7 factors weighed heavily
in physician decisions, in descending order: previous intracerebral
hemorrhage, anticoagulation use, NIHSS score, and previous recent
ischemic stroke. However, in a conjoint model, only 25% of the
variability in decision-making was accounted for. The authors also
explored the effect of individual physician characteristics, such as
age, years of practice, sex, and area of training; they found no
significant impact on the probability to use thrombolysis. Overall, a
substantial proportion of the variability in decision-making in minor
stroke remains currently unexplained. See p 1933.
No clue what CE is. But it doesn't say how fast it is or how fast it needs to be to get to 100% recovery after a bleed is stopped. https://www.dotmed.com/news/story/41937
Zebra Medical Vision announced on Monday that it received CE mark for its brain bleed detection algorithm to be integrated into its Deep Learning Imaging Analytics platform.
This is part of the company’s AI1 business model that provides health care providers with access to its current and future algorithms for one dollar per scan.
“This new algorithm is an important addition to Zebra’s Analytics Engine,” says Dr. Mike Phillips, chief of clinical and outreach services at Intermountain Healthcare, said in a statement. “The ability to alert radiologists and surgeons to the presence of brain bleeds is critical, and will bring significant benefits in patient care to health care organizations.”
Since its inception in October, it has grown to offer algorithms for automatically detecting low bone mineral density, vertebral fractures, fatty liver, coronary artery calcium, emphysema and more.
The new algorithm is capable of detecting a type of brain bleed called intracranial hemorrhage, which occurs when there is bleeding inside the skull. Almost six million people die every year from brain bleed-related conditions, according to the World Stroke Organization.
This is Zebra Medical’s first acute care algorithm. The company plans to deploy it for point of care detection and work list prioritization, so radiologists can better manage their workload.
In the coming months, the company plans to launch several additional “high impact” algorithms. To date, AI1 has been used to evaluate over one million scans in more than five countries.
Now if we could just get some followup on this which LEADERS would accomplish. But we have none. Ask your stroke hospital president whom the LEADERS are in stroke and what they are doing that makes them LEADERS. Now we just need to find out exactly how much time there is to stop that toxicity. There are simple steps to solve this problem. Damn it all, this is so easy to solve, RFPs to researchers and they will come up with answers.
by University Of Texas Health Science Center At Houston
White
blood cells called neutrophils are like soldiers in your body that form
in the bone marrow and at the first sign of microbial attack, head for
the site of injury just as fast as they can to neutralize invading
bacteria or fungi using an armament of chemical weapons.
But when that injury is an intracerebral hemorrhage, which releases
blood into the brain, neutrophils arrive at the point of battle only to
discover that there's no infection to attack. Unless immediately removed
from the brain by other immune cells, they actually cause damage and
deploy an array of toxic chemicals into the brain that worsen injury.
Now researchers at The University of Texas Health Science Center at
Houston (UTHealth) have discovered a way to temporarily suppress these
soldiers' pro-killing effect and turn them into beneficial weapons that
scavenge for toxins, potentially opening a door for a therapeutic
approach to hemorrhagic stroke treatment.
The results of the preclinical study, led by senior author Jaroslaw Aronowski, M.D., Ph.D., were published today in Nature Communications.
Aronowski is professor, Roy M. and Phyllis Gough Huffington Chair in
Neurology and vice-chair for research in the Department of Neurology at
McGovern Medical School at UTHealth.
A hemorrhagic stroke occurs when an artery inside the brain leaks or
ruptures. It is the second-most common form of stroke after ischemic
stroke, has a 30 to 67 percent mortality rate and is the main cause of
disabilities among adults. Mechanical compression of the brain, caused
by blood leaking from disrupted vessels and injury from the actual blood
products, is the main cause of damage to the brain.
Because half of hemorrhagic stroke victims die within the first two
days, researchers believe that deadly secondary damage, including
through toxicity of iron from the breakdown of red blood cells, leads to
an excess in free radicals and inflammation.
Along with carrying chemicals that could aggravate injury,
neutrophils produce and release potentially beneficial molecules
including lactoferrin, an iron-binding protein.
At the same time the neutrophils are getting ready to attack inside
the brain, the brain and spleen are releasing interleukin-27 molecules,
which can signal to the neutrophils to produce more lactoferrin and thus
benefit the brain as it recovers from the stroke injury.
"This is one of the first discoveries showing that you can train
neutrophils to act as friendly cells. We've adapted how the body already
responds naturally but it can take 12 to 18 hours for the signal to
turn them from damaging neutrophils to the beneficial cells that release
lactoferrin and by then, it can be too late," Aronowski said.
"Treatment with lactoferrin in our models is effective in reducing brain
damage after hemorrhage and we are working on a modified form of
lactoferrin that could penetrate the brain better and quicker."
Fuck, we are fifty years behind in treating any type of stroke and stroke rehabilitation. I blame the complete and total lack of leadership from our fucking failures of stroke associations. Case in point; tPA has a 88% failure rate on complete recovery. This was known immediately in 1996 when approved, yet leadership kept supporting expansion and never acknowledged that failure to the general public. From last years World Stroke Day comes this complete fucking lie. 'Stroke is Treatable'.
Written by Professor Rustam Al-Shahi Salman on 31 August 2017
Fifty years ago, people suffering from a heart attack were
taken to hospital, given pain relief, and doctors then watched and
waited to see whether they would survive. Around 80 per cent didn’t.
Thanks to decades of research, 80 per cent of people now
survive a heart attack. If only the same could be said for stroke due to
brain haemorrhage - when a blood vessel bursts and bleeds into the
brain.
Every ten seconds, someone somewhere in the world has a
brain haemorrhage. Within a year, more than half of these people will
die.
When blood vessels in the brain rupture, it is very
difficult to make the bleeding stop. So far, nine clinical trials
looking at drugs to halt bleeding in the brain have not shown a clear
benefit for patients.
Analysis from the British Heart Foundation this month has
shown us that the number of people dying from a stroke in the UK has
remained static for the last five years. This is despite an increase in
general awareness of stroke symptoms and a rise in stroke sufferers
making it to A&E.
It’s clear that we urgently need more options for patients.
There is no specific emergency treatment for brain haemorrhage. The only
options at our disposal are lowering blood pressure with drugs or - as a
last resort - removing the blood with surgery. But again, several
clinical trials have not shown a clear benefit of these treatments for
patients.
Why is the situation so dire for stroke patients? Clinical
trials looking at treatments for brain haemorrhage are notoriously
difficult to conduct. Death rates are high and those who do survive are
often left with life-long disabilities, meaning the pool of people we
have to recruit from is small.
Clinical trials are also expensive. The total overall
research funding by charities and government into stroke is small when
compared to the death and disability that it causes - in 2012 the total
research spend on stroke was less than half the comparable spend on
dementia or cancer. We’re going to need to see more investment into
stroke research if we want to change the story for people who’ve had a
stroke.
Despite the challenges, it may be that patients provide some
of the solutions, and can help us to bring brain haemorrhage treatment
into the 21st century.
Since 2010, the LINCHPIN study in Edinburgh has been
collecting a bank of brains from people who die after brain haemorrhage.
So far, more than 130 people who’ve had a brain haemorrhage have
bequeathed their brains to us after their death. We use the brain tissue
to understand the causes and consequences of brain haemorrhage. This
could help to identify new treatments.
Next, we want to look at the role that inflammation - caused
by brain tissue coming into contact with blood during a stroke – may
play in helping or hindering recovery. There are many treatments for
inflammation, but we don’t know which ones to use after brain
haemorrhage. Hopefully, this will lead to clinical trials of a treatment
for inflammation that may improve outcome for people with brain
haemorrhage.
My research programme at the University of Edinburgh is
called RUSH - Research to Understand Stroke due to Haemorrhage. It’s a
fitting acronym, because we are quite literally in a rush – a race
against time driven by an ageing population who are prone to brain
haemorrhage. Until we find a way to treat brain haemorrhage the number
of people dying or suffering long-term disability is only going to
increase. Professor Rustam Al-Shahi Salman is Personal Chair of
Clinical Neurology at the University of Edinburgh. He leads the Research
to Understand Stroke due to Haemorrhage (RUSH) programme
No mention of doing anything about the hemorrhage cascade of death. There should be no amount of luck in any intervention for stroke. The protocols should all be publicly available with efficacy percentages. The goal is 100% recovery for all stroke patients regardless of when intervention starts. That should be possible when neurogenesis and neuroplasticity are fully understood and documented on how to recovery functionality. Yes these are the BHAGs(Big Hairy Audacious Goals)problems in stroke. If your doctor and stroke hospital are not trying to solve these they need to be shot.
It was a perfectly normal day. Cathy Alexander was starting the new
year by visiting her mom in Cleveland—two hours away from her home in
Columbus, Ohio. They were having coffee and an enjoyable breakfast
before Cathy would start on her way back home. Cathy’s husband, Mike,
was traveling in Alabama as part of his typical work demands.
Being away from home on that foggy, rainy winter day on Jan. 12 was not
that unusual. Cathy visited her mom quite often. But this trip would
end very different from past visits.
“She went to get up from the table and the plate she was holding
dropped to the floor,” said Cathy’s mom, Lorre Andryszczyk. “There were
no symptoms, no complaints, no signs of anything being wrong. Then she
said, ‘I hope I’m not having a stroke.’ I immediately called 9-1-1.”
Cleveland’s mobile stroke unit responded to the call and Cathy had her
first brain scan before reaching the hospital that was only minutes
away. She arrived at the emergency department awake, but confused and
with difficulty speaking and moving the right side of her body.
Cathy had a hemorrhagic stroke with what a Cleveland hospital
neurosurgeon called a medium to moderate size hemorrhage located deep in
the basil ganglia area on the left side of her brain.
“This is an area where we have typically not been able to do surgery
due to the deep location,” the neurosurgeon said. “But Cathy was
absolutely the ideal candidate for a new surgical approach we had been
using for about two years.”
Before surgery could begin, however, the neurosurgeon would need the
approval of Cathy’s husband. Mike recalls the telephone conversation
being very direct. “The options were to do nothing or consent to a new
kind of brain surgery for stroke using new technology called BrainPath.
“If they didn’t do the BrainPath procedure, I knew the outcome would
not be good and this story would have a completely different ending,”
Mike said. “So I agreed to the surgery. The nurse promised they would
take really good care of Cathy, and I jumped on a plane for Cleveland.”
The neurosurgeon had performed more than 60 surgeries using the
BrainPath Approach, a minimally-disruptive kind of brain surgery that
uses the NICO BrainPath to access the hematoma by creating a path
through the natural folds of the brain to evacuate the clot. More than
5,000 surgical procedures have been performed using the technology, and
this local hospital was among the first in the country to have the
technology. “I
had very pessimistic thoughts during my time in flight,” Mike
remembers. “I didn’t have any experience with stroke, but I knew this
was serious. I wondered if I would ever see my wife alive again.”
As with any kind of stroke, time was precious. It was just over two
hours after Cathy’s stroke when she was wheeled into the OR. The surgeon
said before the availability of BrainPath, patients like Cathy would
have been stabilized in the ICU and then a “watch and wait” approach
would have been taken to allow the brain to absorb the blood.
“Many times this resulted in a long and drawn out recovery with
complications that included brain swelling, possible surgery because of
swelling and longer ICU stays,” said the surgeon. “Hemorrhagic stroke,
even today, is not considered a surgical disease. But the BrainPath has
given us the option to go after this kind of clot.
“We didn’t operate before,” he added. “Five years ago, I would not have
operated at all on this kind of stroke. It’s taken us two years of
using the system and getting comfortable. Now we’ve seen the results
with BrainPath, and it’s really changing our thinking on this.”
Cathy’s surgery was completed in less than two hours. Cathy’s mom said
the nurse gave her two thumbs up when they wheeled Cathy out of surgery.
“Cathy immediately smiled at us. She was talking and she recognized
us,” Lorre said. “I knew then that my daughter would be fine.”
After surgery, the surgeon said he was really amazed at how well and
how quickly Cathy was recovering. “As soon as she woke up, she was
brighter and started to speak immediately.
“Hemorrhagic stroke is a very, very difficult disease,” the surgeon
said. “Some of the brain is always affected. Recovery of 100 percent is a
lofty goal, but certainly, that’s what we are here to do.”
Cathy was in the hospital for nine days and rehabilitation for 17 days.
“There hasn’t been one person who hasn’t been impressed and astonished
at how well I’m doing,” Cathy said. “People say they don’t even know
I’ve had a stroke.”
Mike attributes Cathy’s survival and recovery to a perfect alignment of
the stars that day in January. If she wasn’t in Cleveland or if she had
already left on the drive from Cleveland to Columbus – it’s nothing
short of a miracle, he said.
“There’s no disputing that without the BrainPath procedure, our life
would have been completely different – and not in a positive way,” Mike
added. “The more I’ve checked into the procedure and talked about it,
it’s fascinating to me. I take a look at Cathy today and we’re so
blessed.”
Cathy is continuing therapy and goes once a week for rehabilitation.
She says they tell her it will take one to two years to reach her
plateau. But that’s not what Cathy believes.
“I’m going to set the new norm,” she said. “I’m on the road to normal.
I’m living more independently than I thought I would. I’m really
grateful for what I have, and it’s only been four months.”
Cathy has healed cosmetically, too. The small, one-inch incision has healed to be invisible, she said.
“As traumatic as this has been, it’s really quite fascinating,” Mike
said. “If it happens to a loved one of yours, pray that you’re at a
place that can do this for you. Literally, it’s that simple.
“I don’t want to sound cliché, but this technology and the choice to
have surgical intervention has to become more available – this just has
to become a more accepted procedure.” For more patient stories on NICO BrainPath visit www.niconeuro.com/patients/.
Hemorrhagic Stroke Clinical Trial
Twenty four healthcare institutions including a prominent Cleveland
hospital, are participating in a randomized controlled trial evaluating
the clinical effectiveness of early surgical intervention using
BrainPath following spontaneous intracerebral hemorrhage (ICH), the
deadliest, costliest and most debilitating form of stroke.
The ENRICH (Early MiNimally-invasive Removal of ICH)
trial is designed to determine the procedural safety, as well as the
economic and functional benefit, of early surgical removal of
intracerebral hemorrhage using the BrainPath Approach compared to the
medical management standard of care. The BrainPath Approach uses a
combination of technologies, including the FDA-cleared NICO BrainPath® or non-disruptive access and NICO Myriad® to achieve the goal of maximum clot evacuation.
The BrainPath device is used to access the hemorrhage site by navigating through the natural folds and fiber tracks of the
brain, displacing brain tissue as it creates a corridor to the
hemorrhage site and evacuating the clot, all through an opening the size
of a dime. Ideal trial candidates are spontaneous supratentorial ICH
patients with a good clinical chance of benefiting from the surgical
treatment based on well-defined criteria for study enrollment.
This trial will build on current peer-reviewed clinical data on the BrainPath Approach including the results1
of a multi-center pilot study presented at the 2015 International
Stroke Conference. The study was on the safety and efficacy of hematoma
evacuation using a trans-sulcal surgical approach with BrainPath and
showed “statistically significant” improvement in patients’ neurological
state associated with early intervention. This improvement was reported
in 35 patients at 10 centers with outcomes showing 89 percent clot
evacuation and no new surgical deficits or deaths and was cited as a
breakthrough in the treatment of hemorrhagic stroke.
“We are hoping this trial is positive so we can be more aggressive
about how we care for people with intracerebral hemorrhage,” said Dr.
Bain, the principle site investigator for the ENRICH trial. “We deal
with this disease so conservatively now, and we can do better. We want
to change the paradigm and treatment of this disease. A standardized
approach and better technology is really going to help us.”
For more information about the ENRICH trial and to learn more about patient criteria for the trial, visit www.ENRICHtrial.com. Learn more about the NICO BrainPath and its use for accessing hemorrhagic stroke by visiting the website at www.NICOneuro.com. Procedure videos showing atraumatic access with BrainPath can be found on YouTube at NICOneuroCorp.
1Labib M, et al. The safety and efficacy of image-guided trans-sulcal
radial corridors for hematoma evacuation: a multicenter study. Late
breaking oral presentation LB12 at: 2015 International Stroke
Conference; February 11-13, 2015; Nashville, TN.
The 411 on Hemorrhagic Stroke
Hemorrhagic stroke results from a weakened vessel that ruptures and
bleeds into the surrounding brain. Studies show that early removal of
the blood can potentially mitigate brain injury.1 However, the current
standard of care calls for medical management of the patient or a “watch
and see” protocol that often allows blood to remain in the brain2.
Hemorrhagic stroke (ICH), impacts more than 160,000 people in the U.S.
and 3.4 million people worldwide.
The Deadliest Form of Stroke
• Accounts for 10-15 percent of all strokes (or ~1/10)
• Early Mortality (30 days) can be up to 50 percent (30-50 percent)
• Only 20 percent of survivors are functionally independent
*All cited: Adeoye, O. and Broderick, J.P. Nat. Rev. Neurol. 6, 593-601
(2010);published online 28 September 2010;
doi:10.1038/nrneurol.2010.146
New Outcomes with BrainPath
• Zero surgical related mortalities
• Immediate, post-procedure improvement in level of consciousness
• 63 percent of patients living functionally independent
(Labib,MA, et al. The Safety and Feasibility of Image-Guided
BrainPath-Mediated Transsulcul Hematoma Evacuation: A Multicenter Study,
Neurosurgery (2017) 80 (4): 515-524. DOI: https://doi.org/10.1227/NEU.0000000000001316 The National Stroke Association provides educational information
about treatments for post-stroke issues through real-life stories.
Promotion of these stories does not imply endorsement of any product or
service and it is recommended that patients ask a healthcare
professional before using any product, medicine, or therapy.
Intracranial
haemorrhages, including intracerebral haemorrhage (ICH),
intraventricular haemorrhage (IVH) and subarachnoid haemorrhage (SAH),
are leading causes of morbidity and mortality worldwide. In addition,
haemorrhage contributes to tissue damage in traumatic brain injury
(TBI). To date, efforts to treat the long-term consequences of cerebral
haemorrhage have been unsatisfactory. Incident rates and mortality have
not showed significant improvement in recent years. In terms of
secondary damage following haemorrhage, it is becoming increasingly
apparent that blood components are of integral importance, with
haemoglobin-derived iron playing a major role. However, the damage
caused by iron is complex and varied, and therefore, increased
investigation into the mechanisms by which iron causes brain injury is
required. As ICH, IVH, SAH and TBI are related, this review will discuss
the role of iron in each, so that similarities in injury pathologies
can be more easily identified. It summarises important components of
normal brain iron homeostasis and analyses the existing evidence on
iron-related brain injury mechanisms. It further discusses treatment
options of particular promise.
![author['full_name']](https://clf1.medpagetoday.com/media/images/author/nicoleLou_188.jpg)
Jun 01 2017
“I
had very pessimistic thoughts during my time in flight,” Mike
remembers. “I didn’t have any experience with stroke, but I knew this
was serious. I wondered if I would ever see my wife alive again.”
the
brain, displacing brain tissue as it creates a corridor to the
hemorrhage site and evacuating the clot, all through an opening the size
of a dime. Ideal trial candidates are spontaneous supratentorial ICH
patients with a good clinical chance of benefiting from the surgical
treatment based on well-defined criteria for study enrollment.