Use the labels in the right column to find what you want. Or you can go thru them one by one, there are only 34,264 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.
Of course your anxiety will be off the charts since you know that if a hemorrhagic stroke occurs you know your doctor HAS NOTHING GUARANTEED FOR RECOVERY!
Postdiagnostic anxiety and depression’s impact on management and outcomes in patients with unruptured intracranial aneurysms remains underexplored. We assessed associations with treatment patterns and outcomes using a large multi-institutional database.
METHODS:
This retrospective cohort study used TriNetX Global Collaborative Network records (2015–2025; >130 million patients across ≈250 health care organizations), identifying 127 361 adults with unruptured intracranial aneurysms. Addressing immortal time bias, we used a 127-day landmark analysis (median time to psychiatric diagnosis), requiring event-free survival before cohort assignment. Of 119 211 patients surviving to the landmark, those with anxiety/depression diagnosed within 0 to 127 days (n=7250) were 1:1 propensity score matched to controls (n=111 961), yielding 6800 per cohort. Cox proportional hazards models evaluated outcomes from a landmark.
RESULTS:
Matched cohorts (6800 each) had balanced characteristics (all standardized mean differences <0.10) and comparable follow-up (median, 1550 versus 1600 days). Anxiety/depression was associated with higher all-cause mortality (6.3% versus 4.5%; hazard ratio [HR], 1.28 [95% CI, 1.11–1.48]; P<0.001) and rupture (3.1% versus 2.2%; HR, 1.33 [95% CI, 1.08–1.64]; P=0.007). Five-year survival was 93.7% in the anxiety/depression cohort versus 95.5% in matched controls. Preventive treatment showed nonsignificant trends toward lower rates (odds ratio, 0.80 [95% CI, 0.62–1.03]; P=0.082). Sensitivity analysis using a 365-day landmark (n=10 200 per cohort) expanded eligibility by including diagnoses between days 128 and 365, and confirmed findings (mortality HR, 1.22 [95% CI, 1.08–1.38]; rupture HR, 1.28 [95% CI, 1.08–1.52]). Fine-Gray competing risk models yielded consistent results (mortality subdistribution HR, 1.27; rupture subdistribution HR, 1.31). Dose-response patterns emerged for psychiatric medication adherence: low (mortality HR, 1.50 [95% CI, 1.12–2.00]; P=0.006), moderate (HR, 1.29 [95% CI, 0.98–1.70]; P=0.071), and high (HR, 1.16 [95% CI, 0.89–1.51]; P=0.270). E values were 1.88 for mortality and 1.99 for rupture.
CONCLUSIONS:
Postdiagnostic anxiety and depression are associated with increased rupture risk and mortality in patients with unruptured intracranial aneurysms. Residual confounding cannot be excluded. These findings require further investigation to establish causality and suggest that an integrated psychiatric assessment may be considered in unruptured intracranial aneurysm management.
Inflammation
has emerged as a key component of the pathophysiology of intracranial
aneurysms. Mast cells have been detected in human intracranial aneurysm
tissues, and their presence was associated with intramural
microhemorrhage and wall degeneration. We hypothesized that mast cells
play a critical role in the development of aneurysmal rupture, and that
mast cells can be used as a therapeutic target for the prevention of
aneurysm rupture.
Methods:
Intracranial
aneurysms were induced in adult mice using a combination of induced
systemic hypertension and a single injection of elastase into the
cerebrospinal fluid. Aneurysm formation and rupture were assessed over 3
weeks. Roles of mast cells were assessed using a mast cell stabilizer
(cromolyn), a mast cell activator (C48/80), and mice that are
genetically lacking mature mast cells (KitW-sh/W-sh mice).
Results:
Pharmacological
stabilization of mast cells with cromolyn markedly decreased the
rupture rate of aneurysms (80% versus 19%, n=10 versus n =16) without
affecting the aneurysm formation. The activation of mast cells with
C48/80 significantly increased the rupture rate of aneurysms (25% versus
100%, n=4 versus n=5) without affecting the overall rate of aneurysm
formation. Furthermore, the genetic deficiency of mast cells
significantly prevented aneurysm rupture (80% versus 25%, n=10 versus
n=8, wild-type versus KitW-sh/W-sh mice).
Conclusions:
These
results suggest that mast cells play a key role in promoting aneurysm
rupture but not formation. Stabilizers of mast cells may have a
potential therapeutic value in preventing intracranial aneurysm rupture
in patients.
Introduction
Rupture
of intracranial aneurysms causes aneurysmal subarachnoid hemorrhage.
The 30-day mortality rate after aneurysmal subarachnoid hemorrhage can
be as high as 45%.1
Therefore, surgical clipping or endovascular coiling are offered to
patients with unruptured aneurysms for the prevention of aneurysmal
rupture. Significant technical advancements and refinements have been
made in these invasive treatments. However, the adverse outcome rates
resulting from the clipping and coiling of unruptured aneurysms are
still not negligible.2
Therefore, pharmacological prevention of aneurysmal rupture may be an
attractive alternative approach in patients with unruptured aneurysms.3
Inflammation is increasingly recognized as a critical component in the pathophysiology of intracranial aneurysms.4–9
Observational studies have shown the presence of inflammatory cells and
inflammatory markers in human intracranial aneurysm tissues and serum
samples.5,10 Mast cells have been detected in human intracranial aneurysm tissues,7,11
and the presence of mast cells was associated with intramural
microhemorrhage and wall degeneration of human intracranial aneurysms.11
Mast
cells, classically known as key regulators of allergic reactions, have
emerged as integral players in cardiovascular diseases.12–17
By releasing cytokines, including tryptase, chymases, cathepsins, and
interleukins, mast cells can affect vascular inflammation and
remodeling.12,18–20
Blocking the cytokine release from mast cells reduces the development
and progression of atherosclerosis and abdominal aortic aneurysm in
animals.14,16 Although previous studies suggested an association between mast cell activation and pathological remodeling of aneurysm walls,21,22
the direct link between mast cell activation and the development of
aneurysmal rupture has not been established. Therefore, we tested
whether mast cells contribute to the development of aneurysmal rupture
using the genetic and pharmacological tools in a mouse model of
intracranial aneurysm.
by Kristin Jenkins, Contributing Writer, MedPage Today
This article is a collaboration between MedPage Today® and:
Action Points
Note that this
systematic review of the literature suggests that small, unruptured
intracerebral aneurysms of less than 7 mm are unlikely to grow and
rupture.
Of course, the rate of rupture of these small aneurysms
is not zero, implying that tailoring surveillance based upon patient
factors is reasonable.
Growth
and rupture rates in small unruptured intracranial aneurysms (UIAs)
appeared to be relatively low, but the quality of published evidence is
poor and current guidelines may need to consider specific follow-up
imaging recommendations, researchers said.
A systematic literature review found that the annual growth rate for
aneurysms 7 mm or smaller was less than 3% in all but one study,
reported Ajay Malhotra, MD, of the Yale School of Medicine in New Haven,
Conn., and colleagues.
In
25 out of 26 studies, the annualized rupture rate for aneurysms 3 mm or
smaller was 0%, less than 0.5% for aneurysms 3 to 5 mm, and less than
1% for aneurysms 5 to 7 mm, they wrote online in the Annals of Internal Medicine.
"Our review highlights that studies had substantial heterogeneity in
imaging frequency and duration, as well as in growth and rupture rates
of UIAs 7 mm and smaller," they noted.
There was only one study
with long-term follow-up, the authors stated with most studies having a
mean follow-up of less than 5 years. The limited evidence indicates
that "better literature is needed, including standardization of the
definition of growth and the criteria used to treat small aneurysms."
For patients treated without surgery or endovascular coiling, current 2015 guidelines
from the American Heart Association/American Stroke Association
recommend a first follow-up study at 6 to 12 months after initial
discovery, with annual or biannual follow-up. No specific
recommendations are made for small UIAs.
"These guidelines may have to consider follow-up imaging
recommendations specifically for small aneurysms (≤3 mm, ≤5 mm, and ≤7
mm), given their very low rupture rate and the poorly understood
correlation between growth and rupture," the authors suggested.
For
the study, MEDLINE, EMBASE, Scopus, and the Cochrane Library databases
from inception to 2017 were searched for published case series and
observational studies reporting natural history data on UIAs 7 mm and
smaller. Out of 26 full-text articles, only 10 reported both growth and
rupture rates, and many excluded patients considered to be at high risk
for rupture.
Follow-up imaging methods (MRI, CT, and cerebral angiography) were
inconsistent across all 26 studies. In 14 studies, follow-up didn't
account for patients with more than one aneurysm. Information on the
frequency and duration of follow-up was insufficient to draw
conclusions.
The results suggest that very small (≤3 mm) and small (3 to 5 mm)
aneurysms have different growth and rupture rates. Since UIAs weren't
categorized by precise size in several studies, however, the authors
were unable to divide them into mutually exclusive subgroups. Instead,
they concluded that the rupture risk of aneurysms 5 to 7 mm was likely
greater than that of UIAs 5 mm and smaller.
The risk factors for growth appeared to be consistent with those for
rupture, according to the authors, noting that predictors of rupture
risk in UIAs 5 mm and smaller may include initial aneurysm size,
posterior circulation and anterior communicating artery location, and size ratio.
Small aneurysms may rupture infrequently but they can also cause
subarachnoid hemorrhage, they pointed out. In 5- to 6-mm aneurysms, the
rupture rate was 1.1% and aneurysms with a daughter sac that were
located in the posterior or anterior communicating artery were more
likely to rupture.
A
study limitation was the high selection bias with regard to treatment
of higher risk aneurysms in the reviewed research. Also the definition
for growth varied between the reviewed studies.
In an accompanying editorial,
Robert M. Starke, MD, from the University of Miami Miller School of
Medicine, warned against concluding from this study "that small
aneurysms have no risk for rupture but rather that experts are skilled
at predicting which aneurysms are more likely to rupture."
Although subarachnoid hemorrhage accounts for only a small percentage
of strokes, its impact can be catastrophic, thanks to a "predilection
for a relatively young population and the poor outcomes in these
patients," Starke pointed out. Almost 25% of potential life-years lost
because of stroke are the result of subarachnoid hemorrhage, he noted.
Patients with aneurysms should undergo expert evaluation that
includes a review of associated risk factors to "determine both the
optimal follow-up plan (if any) and the need for treatment," said
Starke, noting that the mortality rate in patients with a ruptured
aneurysm is about 50%.
This review "should prompt better prospective observational studies," he stated.
Robert
D. Brown Jr., MD, MPH, of the Mayo Clinic in Rochester, Minn., agreed.
The risk of growth and/or rupture for smaller aneurysms may be low but
it isn't zero. Rupture risk prediction, and treatment recommendations
should be individualized," he told MedPage Today in an email.
Brown, who was not involved in the study, noted that study provides a
good summary of available data. He pointed out that aneurysm location
and morphology are also important predictors of growth and rupture.
Family history and selected risk factors such as smoking or hypertension
may also be important predictors of aneurysm growth.
"These aneurysms are relatively commonly seen in clinical practice,
often detected on brain imaging performed for other, unrelated reasons.
The key question after the aneurysm is detected is whether the aneurysm
requires interventional treatment, and if not, how should it best be
followed," he said.
Since it can be difficult to determine the stability of small
aneurysms, follow-up with CT angiography and MR angiography "should be
considered for unruptured aneurysms that are treated conservatively,"
Brown said.
The issue of potential utility of medical management "is an important
one," he added, "given that there are some data to suggest that aspirin
may be effective in lowering the risk of rupture. Management of high
blood pressure, and assistance with smoking cessation may be important
too."
Malhotra and
Starke disclosed no relevant relationships with industry. One co-author
disclosed a relevant relationship with Philips Healthcare.
Reviewed by
F. Perry Wilson, MD, MSCE
Assistant Professor, Section of Nephrology, Yale School of Medicine
and Dorothy Caputo, MA, BSN, RN,
Nurse Planner
BACKGROUND
AND PURPOSE Subarachnoid hemorrhage after intracranial aneurysm rupture
remains a serious condition. We performed a case-control study to
evaluate the use of computed hemodynamics to detect cerebral aneurysms
prone to rupture.
METHODS Four patients with incidental aneurysms that ultimately
ruptured (cases) were studied after initially being included in a
prospective database including their 3-dimensional imaging before
rupture. Ruptures were located in different arterial segments: M1
segment of the middle cerebral artery; basilar tip; posterior inferior
cerebellar artery; and anterior communicating artery. For each case, 5
controls matched by location and size were randomly selected. An
empirical cumulative distribution function of aneurysm wall shear stress
percentiles was evaluated for every case and used to define a critical
prone-to-rupture range. Univariate logistic regression analysis was then
used to assess the individual risk of rupture.
RESULTS A cumulative wall shear stress distribution characterizing a
hemodynamic prone-to-rupture range for small-sized aneurysms was
identified and fitted independent of the location. Sensitivity and
specificity of the preliminary tests were 90% and 93%, respectively.
CONCLUSIONS The wall shear stress cumulative probability function may be a potential predictor of small-sized aneurysm rupture.
A
Temple bioengineer is collaborating on an NIH-funded project to develop
a nanotechnology that will help doctors determine the location and
severity of plaques in artery walls before they rupture.
Atherosclerosis, or hardening of the arteries, occurs when fat,
cholesterol, calcium and other substances form such plaques. The disease
is a major cause of heart attacks and strokes when these plaques
rupture and form clots in the blood.
Omar Z. Fisher, assistant professor of bioengineering in Temple’s
College of Engineering, has developed a method for linking polyphenols,
which are very strong antioxidants, to polymers that can self-assemble
into nanoparticles.
Fisher said the project will focus on using these polymers to
encapsulate superparamagnetic iron oxide particles (SPIOs), a nano-scale
MRI contrasting agent used by his collaborator, Amber Doiron, assistant
professor of bioengineering at Binghamton University.
The antioxidant nanoparticles containing the contrasting agent would
travel through the blood vessels until they reach atherosclerotic
plaque, enabling doctors to diagnose the severity of plaques before they
rupture, said Fisher.
“The worse the plaque is, the more likely it is to rupture and give
you a clot,” he said. “Because these polymers are made from
antioxidants, they are sensitive to oxidative stress, which is more
prevalent in more severe plaques.”
Once the oxidative stress destroys the polymers, the MRI contrast agents will be released inside the plaques.
Fisher said doctors would likely prescribe an MRI when a patient was
showing some signs of cardiac distress such as fatigue or chest pains.
“During the MRI, the degree of contrast would be visible and indicate
to doctors not only that the plaques were there, but the severity of
the plaques and how likely they would be to rupture,” he said.
The project is supported through a two-year, $418,000 grant which
Fisher and Doiron recently received from the National Institute for
Biomedical Imaging and Bioengineering.
Are Cryptogenic Strokes Really Cryptogenic?
More than one-third of patients who had a stroke of unknown origin
were found to have complex carotid plaques in nonstenosed arteries,
according to a small study.
MR imaging showed the prevalence of complicated type VI plaques,
according to American Heart Association classification, in 12 of 32
carotid arteries ipsilateral to the stroke, compared with no such
findings in the contralateral arteries, reported Tobias M. Freilinger,
MD, from Ludwig-Maximilians-University Munich, and colleagues.
In three-quarters of the plaques, intraplaque hemorrhage was the most
common diagnostic feature, followed by fibrous plaque rupture in 50%,
and surface thrombus in 33%, according to results published in this
month's JACC: Cardiovascular Imaging.
"The realization that even apparently 'minor' atherosclerosis may
harbor high-risk disease should change our perception of what
constitutes risk for a patient," wrote Alan Moody, MD, from Sunnybrook
Health Sciences Center in Ontario, Canada, in an accompanying editorial.
Also reported in the journal, Alistair C. Lindsay, MBChB, from the
University of Oxford in the U.K., and colleagues found that slightly
more than half of 41 patients who suffered a transient ischemic attack
had type VI plaques compared with eight asymptomatic controls.
Lindsay's group identified the three most common features as
intraplaque hemorrhage, cap rupture, and surface thrombus. These
features were in carotid arteries that were not considered significantly
stenotic.
They also found that only two plaques showed signs of healing at
6-weeks' follow-up. Moody said that "this represents an ongoing source
for thromboemboli and a potential therapeutic target for secondary
prevention."
