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 risk. Show all posts
Showing posts with label hemorrhage risk. Show all posts
The FDA has granted 510(k) clearance to a Bay Area commercial stage
medical technology company for its novel large-bore catheter stroke
thrombectomy system.
In a press release, device manufacturer Imperative Care Inc. said the
Zoom System is “the first comprehensive stroke thrombectomy system to
include large-bore .088 catheters indicated for both access and
aspiration when used with a Zoom Catheter.”
The FDA granted 510(k) clearance to a large-bore stroke thrombectomy catheter system.Image: Adobe Stock
The FDA’s decision is based on data from the prospective, multicenter
Imperative clinical trial, which evaluated the safety and efficacy of
the Zoom catheter system in 211 adult patients with acute ischemic stroke
who received care across 26 sites in the United States. According to
the release, patients were treated with concurrent aspiration
thrombectomy using two catheters.
The Zoom system was associated with a median duration of 19 minutes(Is that fast enough for 100% recovery?) from groin puncture to modified treatment in cerebral infarction score
of at least 2B reperfusion, which is the shortest duration among other
thrombectomy trials, the release said.
The Zoom system was also associated with a core-lab adjudicated rate of symptomatic intracranial hemorrhage
of 0.9% and a rate of independently adjudicated dissection and vessel
perforation of 0.5%, both lower than previous clinical trials, according
to the company.
“We know that with stroke, time is the most critical factor in driving positive patient outcomes,” Ariel Sutton,
executive vice president and general manager of Imperative Care’s
Stroke business, said in the release. “The Zoom system is the first
purpose-built technology from access to aspiration that maximizes
versatility for rapid and effective procedures as validated by the
Imperative trial and previous clinical studies of the Zoom Stroke
Solution.”
Hopefully your doctor isn't using high dose statins due to the FDA safety comments. You doctor has only had 13 years to find out this and implement it!
High-intensity statin therapy may increase bleeding risk after minor stroke.(Why are you researching this? Known for 13 years and your doctors don't follow worldwide research?)
Statin dose, moderate or high, did not appear to have an effect on stroke recurrence.
Initiation of high-intensity statin therapy during the acute phase of
minor, noncardiogenic stroke may increase bleeding risk, according to
the results of a Chinese cohort study published in the Journal of the American Heart Association.
“The 2021 American Heart Association/American Stroke Association
guidelines recommend high-intensity statin therapy for individuals at
high risk for atherosclerotic cardiovascular disease. However, some
randomized controlled trials have demonstrated that among Asian
populations, more aggressive statin-based low-density lipoprotein cholesterol (LDL-C)-lowering treatments did not improve clinical outcomes or reduce the risk of stroke recurrence,” Hai-mei Fan, MD, PhD, from thedepartment
of neurology at First Hospital of Shanxi Medical University in Taiyuan,
China, and colleagues wrote. “Therefore, it is unknown whether Asian
populations benefit more from intensive statin therapy for secondary stroke prevention.”
High-intensity statin therapy may increase bleeding risk after minor stroke. Image: Adobe Stock
For the secondary report from the SEACOAST study, Fan and colleagues
analyzed outcomes data from 2,950 patients with mild ischemic stroke who
presented within 72 hours of symptom onset to eight hospitals in Shanxi
province, China.
Moderate or intensive statin dose was defined in accordance with the
2018 AHA/American College of Cardiology cholesterol guideline.
Daily rosuvastatin 20 mg or atorvastatin 40 mg to 80 mg were
considered high-intensity statin treatments. Daily atorvastatin 10 mg to
20 mg, rosuvastatin 5 mg to 10 mg, simvastatin 20 mg to 40 mg,
pitavastatin 2 mg to 4 mg or pravastatin 40 mg to 80 mg were considered
moderate-intensity statin treatments.
The primary efficacy outcome was stroke recurrence and the primary safety endpoint was intracranial hemorrhage.
After adjusting for potential confounders in a matched Cox
multivariate analysis, the researchers found that risk for stroke
recurrence at 3 and 12 months was similar in the high- and moderate-
intensity statin groups (adjusted HR at 3 months = 1.12; 95% CI,
0.85-1.49; P = .424; aHR at 12 months = 1.08; 95% CI, 0.86-1.34; P
= .519). However, high-intensity statin therapy was associated with
increased risk for intracranial hemorrhage compared with
moderate-intensity statin therapy at both time points (aHR at 3 months =
1.81; 95% CI, 1-3.25; P = .048; aHR at 12 months = 1.86; 95% CI, 1.1-3.16; P = .021). It was also associated with elevated risk for any bleeding events (aHR = 1.44; 95% CI, 1.08-1.93; P = .013).
The researchers also utilized propensity-score matching to control
for imbalances in baseline factors, which produced results consistent
with the Cox multivariate analysis.
“This cohort study suggests that compared with moderate-intensity
statin therapy, high-intensity statin medication in the acute period may
not positively influence clinical outcome of patients with minor,
noncardiogenic ischemic stroke,” the researchers wrote. “In practice,
maybe a moderate dosage of statins is appropriate for the secondary
prevention of mild stroke.”
Due to the study being mainly completed during the COVID-19 pandemic,
the researchers noted a lack of follow-up data for variables such as
lipids, liver function, muscle enzymes and kidney function. Lack of
these data prevented the researchers from completing a more
comprehensive analysis of the adverse reaction rate of different statin
doses after minor stroke.
Background and Purpose:
In patients with acute mild-moderate ischemic stroke or high-risk
transient ischemic attack (TIA), the Acute Stroke or Transient Ischemic
Attack Treated with Ticagrelor and Aspirin for Prevention of Stroke and
Death (THALES) trial demonstrated that when added to aspirin, ticagrelor
reduced stroke or death but increased risk of severe hemorrhage
compared with placebo. The primary efficacy outcome of THALES included
hemorrhagic stroke and death, events also counted in the primary safety
outcome. We sought to disentangle risk and benefit, assess their
relative impact, and attempt to identify subgroups with disproportionate
risk or benefit.
Methods: In a randomized,
placebo-controlled, double-blind trial of patients with mild-to-moderate
acute noncardioembolic ischemic stroke or high-risk TIA, patients were
randomized within 24 hours after symptom onset to a 30-day regimen of
either ticagrelor plus aspirin or matching placebo plus aspirin. For the
present analyses, we defined the efficacy outcome, major ischemic
events, as the composite of ischemic stroke or non-hemorrhagic death,
and defined the safety outcome, major hemorrhage, as intracranial
hemorrhage or hemorrhagic death. Net clinical impact was defined as the
combination of these two endpoints.
Results: In
11 016 patients (5523 ticagrelor-aspirin and 5493 aspirin), a major
ischemic event occurred in 294 patients (5.3%) in the ticagrelor-aspirin
group and in 359 patients (6.5%) in the aspirin group (absolute risk
reduction 1.19%, 95%CI 0.31%-2.07%). Major hemorrhage occurred in 22
patients (0.4%) in the ticagrelor-aspirin group and 6 patients (0.1%) in
the aspirin group (absolute risk increase 0.29%, 95% CI, 0.10-0.48%).
Net clinical impact favored ticagrelor-aspirin (absolute risk reduction
0.97%, 95% CI, 0.08%-1.87%). Findings were similar when different
thresholds for disability were applied and over a range of predefined
subgroups.
Conclusions: In patients with
mild-moderate ischemic stroke or high-risk TIA, ischemic benefits of
30-day treatment with ticagrelor-aspirin outweigh risks of hemorrhage.
First time I've seen mention of hemorrhage risk, not changing my anti-coagulation strategy. I didn't have any bleed problems after my tPA dose so I think I'm good, no problems with a couple of Lovenox shots either.
with associated hemorrhagic lesions in 11/37
patients.
Brain MRI parenchymal signal abnormalities have been in association with SARS-CoV-2.
Purpose
Describe
the neuroimaging findings (excluding ischemic infarcts) in
patients with severe COVID-19 infection.
Methods
This
was a retrospective study of patients evaluated from March 23th,
2020 to April 27th, 2020 at 16 hospitals.
Inclusion criteria were: (i) positive
nasopharyngeal or lower respiratory tract reverse
transcriptase-polymerase chain reaction assays; (ii) severe COVID
infection defined as requirement for
hospitalization and oxygen therapy; (iii)
neurologic manifestations; (iv) abnormal brain MRI. Exclusion
criteria were patients with missing or
non-contributory data regarding brain MRI or
a brain MRI showing ischemic infarcts, cerebral venous
thrombosis, or chronic lesions unrelated to the current
event. Categorical data were compared using
Fisher exact test. Quantitative data were
compared using Student’s t-test or Wilcoxon test. A
p-value lower than 0.05 was considered significant.
Results
Thirty
men (81%) and 7 women (19%) met inclusion criteria, with a mean
age of 61+/- 12 years (range: 8-78). The most
common neurologic manifestations were
alteration of consciousness (27/37, 73%),
pathological wakefulness when the sedation was stopped (15/37, 41%),
confusion (12/37, 32%), and agitation (7/37,
19%). The most frequent MRI findings were:
signal abnormalities located in the medial temporal lobe
in 16/37 (43%, 95% CI 27-59%) patients, non-confluent
multifocal white matter hyperintense lesions
on FLAIR and diffusion sequences, with
variable enhancement, with associated hemorrhagic lesions in 11/37
patients (30%, 95% CI 15-45%), and extensive and
isolated white matter microhemorrhages in
9/37 patients (24%, 95% CI 10-38%). A majority of
patients (20/37, 54%) had intracerebral hemorrhagic lesions with a
more severe clinical presentation: higher
admission rate in intensive care units,
20/20 patients, 100% versus 12/17 patients, 71%, p=0.01;
development of the acute respiratory distress syndrome in
20/20 patients, 100% versus 11/17 patients,
65%, p=0.005. Only one patient was positive
for SARS-CoV-2 RNA in the cerebrospinal fluid.
Conclusion
Patients
with severe COVID-19 and without ischemic infarcts had a wide
range of neurologic manifestations that were be
associated with abnormal brain MRIs. Eight
distinctive neuroradiological patterns were
described.
Summary
Eight
distinctive neuroradiologic patterns (excluding ischemic infarcts) were
identified in patients with severe COVID-19
infection with abnormal brain MRIs.
Key Results
1.
In patients with COVID-19, the most frequent neuroimaging features
were: involvement of the medial temporal lobe,
non-confluent multifocal white matter
hyperintense lesions on FLAIR with variable enhancement and
hemorrhagic lesions, and extensive and isolated white
matter microhemorrhages.
2.
A majority of our patients presented intracerebral hemorrhagic
lesions, which were associated with worse clinical
status.
3. Of 37 patients, only one was positive for SARS-CoV-2 RNA in the cerebrospinal fluid.
Introduction
SARS-CoV-2 is the seventh member of the family of coronaviruses (CoVs) that infect humans (1)
and induces COVID-19 disease. Human CoVs (HCoVs) have
neuroinvasive capacities and may be neurovirulent by two main
mechanisms (2-4):
viral replication into glial or neuronal cells of the brain, or
autoimmune reaction with a misdirected host immune response (5). Thus, a few cases of acute encephalitis-like syndromes with hCoVs were reported in the past two decades (5-8). Concerning COVID-19, current data on central nervous system (CNS) involvement is uncommon but growing (9-17), demonstrating the high frequency of neurological symptoms.
However,
the delineation of a large cohort of confirmed brain MRI parenchymal
signal abnormalities (excluding ischemic infarcts)
related to COVID-19 has never been performed, and the
underlying pathophysiological mechanisms remain unknown. The
purpose of this current study was to describe the neuroimaging
findings (excluding ischemic infarcts) in patients with
severe COVID-19 and report the clinico-biological
profile of these patients.
Material & Methods
This
retrospective observational national multicenter study was initiated by
the French Society of Neuroradiology (SFNR) in
collaboration with neurologists, intensivists, and
infectious disease specialists, and brought together 16 hospitals.
The study was approved by the ethical committee of Strasbourg
University Hospital (CE-2020-37) and was in accordance
with the 1964 Helsinki Declaration and its later
amendments. Due to the emergency in the context of COVID-19 pandemic
responsible for acute respiratory and neurological
manifestations pandemic, the requirement for patients’
written informed consent was waived.
Patient cohort
Consecutive
patients with COVID-19 infection and neurologic manifestations who
underwent brain MRI were included from March 23th, 2020, to April 27th,
2020, in 16 French centers, including 11 university
hospitals and 5 general hospitals. Inclusion criteria were: (i)
diagnosis of COVID-19 based on possible exposure
history or symptoms clinically compatible, validated
with a detection of SARS-CoV-2 by reverse transcriptase-polymerase
chain reaction (RT-PCR) assays on the nasopharyngeal,
throat or lower respiratory tract swabs; (ii) severe
COVID-19 infection defined as requirement for
hospitalization and oxygen therapy; (iii) neurologic manifestations;
(iv) abnormal brain MRI with acute/subacute
abnormalities. Exclusion criteria were: (i) patients
with missing or non-contributory data (lack of sequences, numerous
artifacts) regarding brain MRI; (ii) a brain MRI showing
ischemic infarcts, cerebral venous thrombosis, or
chronic lesions unrelated to the current event.
Clinical and laboratory data were extracted from the patients’
electronic medical records in the Hospital
Information System. Only laboratory analysis within
three days before the brain MRI were considered. In the case of
redundancy of the tests, the worst value has been kept.
Clinical and biological data were reviewed by two
neurologists (J.D.S., and M.A. with 25 and 15 years of
clinical expertise on neurology, respectively), and by one virologist
(S.F-K). They participated to the elaboration of
the study design, the interpretation of the data,
and to manuscript editing. When available, all electroencephalogram
(EEG) were reviewed by one expert neurologist (C.B.) and
classified into five groups (normal, under
sedation, nonspecific, encephalopathy or seizures).
Virological assessment
Quantitative
real-time RT-PCR tests for SARS-CoV-2 nucleic acid were performed on
nasopharyngeal or lower respiratory tract swabs, and
cerebrospinal fluid (CSF). Primer and probe
sequences target two regions on the RdRp gene and are specific
to SARS-CoV-2. Assay sensitivity is around 10 copies/reaction
(in house-method, Institut Pasteur, Paris, France) (18).
Brain MRI protocols
Imaging
studies were conducted either on 1.5- or 3-Tesla MRI. The multicenter
nature of the study and the various clinical setups
did not allow standardization of sequences. The most
frequently sequences performed were 3D T1 weighted
spin-echo MRI with and without contrast enhancement, diffusion-weighted
imaging (DWI), gradient-echo T2 or
Susceptibility-weighted imaging, and 2D or 3D FLAIR
after administration of gadolinium-based contrast agent.
MRI interpretation
After
anonymization, images were presented to readers with our GE Picture
Archiving and Communication System (General Electric,
Milwaukee, WI, USA). After review of MRI studies by
three neuroradiologists (S.K., F.C., and F.L. with 20,
25, and 9 years of experience in neuroradiology, respectively) who
were blinded to all patient data, brain MRI findings
were divided by consensus into eight groups: (a)
unilateral FLAIR and/or diffusion hyperintensities located in medial
temporal lobe; (b) FLAIR and diffusion ovoid
hyperintense lesion located in the central part of
the splenium of the corpus callosum; (c) non-confluent
multifocal white matter (WM) hyperintense lesions on FLAIR and
diffusion, with variable enhancement; (d)
non-confluent multifocal WM hyperintense lesions on
FLAIR and diffusion, with variable enhancement, associated with
hemorrhagic lesions; (e) acute necrotizing
encephalopathy (ANE) (9)
when symmetric thalamic lesions (edema, petechial
hemorrhage, and necrosis), with variable involvement of the brainstem,
internal capsule, putamen, cerebral and cerebellar
WM; (f) extensive and isolated WM microhemorrhages;
(g) extensive and confluent supratentorial WM FLAIR
hyperintensities; (h) FLAIR hyperintense lesions involving both middle
cerebellar peduncles. Patients could have had more
than one pattern.
Statistical analysis
Data
were described using frequency and proportion (n, %) for categorical
variables, using mean, median, interquartile range,
and range for quantitative data. In a second step,
patients with hemorrhagic lesions were gathered into a
single group called « patients with hemorrhagic complications », to
look for clinico-biological differences between the
two populations. Categorical data were compared
using Fisher exact test. Quantitative data were compared
using Student’s t-test or Wilcoxon test. A p-value lower than 0.05
was considered significant.
Results
Between March 23th, 2020, and April 27th,
2020, 190 consecutive patients with COVID-19 infection
and neurologic manifestations, performed a brain MRI in
16 hospitals. Among them, were excluded all patients with normal brain
MRI, ischemic infarcts, cerebral venous thrombosis or
chronic lesions unrelated to the current event. A total
of 37 patients with COVID-19 infection were finally included
in this study (figure 1). The average age of the patients was 61 +/- 12 years with 30 men and 7 women included (table 1).
The majority of our patients (32/37, 87%) were admitted
to Intensive Care Units (ICUs) because of acute
respiratory failure. The most frequent neurologic manifestations were
alteration of consciousness (27/37, 73%), pathological
wakefulness after sedation (15/37, 41%), confusion
(12/37, 32%), and agitation (7/37, 19%).
Figure 1. Flowchart of patient inclusion and exclusion
Table 1: Epidemiologic profile and clinical characteristics
Among
the 26 EEG performed, 2 (8%) were considered as normal, 6 (23%) were
realized under sedation, 10 (39%) showed nonspecific
findings, 7 (27%) were classified as encephalopathy, and
1 (4%) case of seizures was also described. At the end of the
study, the mortality rate was 14%. The blood counts of patients
showed leukocytosis, lymphopenia, and anemia. Patients
had elevated serum levels of C-reactive protein,
ferritin, alanine aminotransferase, aspartate aminotransferase, urea,
creatinine, fibrinogen, and D-dimers (table 2).
Fifteen out of the 19 patients (79%) studied for the
presence of a lupus anticoagulant were positive.
Laboratory findings
Table 2: Laboratory findings
Thirty-one
patients underwent a lumbar puncture, and among them, 21/31(68%) had
increased markers of inflammation (high white blood cell
count, and/or high proteinorachia, and/or elevated
immunoglobulin G). One patient demonstrated the presence
of SARS-CoV-2 on RT-PCR. High levels of interleukin-6 were found in 2
out of 6 patients (table 3).
Cerebrospinal fluid analysis
Table 3: Cerebrospinal fluid analysis
Neuroimaging findings
The results of MRI findings are summarized in figure 1.
Among the 37 patients included, 28/37 (76%) were
associated with one neuroimaging pattern, 7/37 (19%) with two patterns,
and 2/37 (5%) showed three patterns (figures 1-6).
The most frequent neuroimaging findings were:
signal abnormalities located in the medial temporal
lobe in 16/37 (43%, 95%IC 27-59%) patients (figure 2),
non-confluent multifocal WM hyperintense lesions on FLAIR
and diffusion, with variable enhancement, associated with
hemorrhagic lesions in 11/37 (30%, 95%IC 15-45%)
patients (figure 3), and in 9/37 (24%, 95%IC 10-38%) patients extensive and isolated WM microhemorrhages were detected (figure 4).
Figure 2.
Axial FLAIR in four different COVID-19 patients. A) 58-year old man
with impaired consciousness: FLAIR
hyperintensities located in the left medial
temporal lobe. B) 66-year old man with impaired consciousness:
FLAIR ovoid hyperintense lesion located in the
central part of the splenium of the corpus
callosum. C) 71-year old woman with pathological
wakefulness after sedation: extensive and confluent supratentorial
white matter FLAIR hyperintensities
(arrows). Association with leptomeningeal
enhancement (stars) D) 61-year old man with confusion: hyperintense
lesions involving both middle cerebellar
peduncles.
Figure 3.
65-year old man with pathological wakefulness after sedation.
Non-confluent multifocal white matter hyperintense
lesions on FLAIR and diffusion, with
variable enhancement, and hemorrhagic lesions. Axial
Diffusion (A, B), Apparent Diffusion Coefficient (ADC) map (C),
axial FLAIR (D, E), sagittal FLAIR (F),
axial Susceptibility weighted imaging (SWI)
(G), and postcontrast T1 weighted MR images (H). Multiple nodular
hyperintense Diffusion and FLAIR lesions localized
in the white matter including the corpus
callosum (F). Some of them (white arrow) are
associated with reduced ADC corresponding to cytotoxic edema (C). Other
lesions are located next to the lenticular
nucleus (cross) (E, G, H), with hemorrhagic
changes (G), and enhancement after contrast
administration.
Figure 4.
57-year old man with pathological wakefulness after sedation. Extensive
and isolated white matter microhemorrhages.
Axial Susceptibility weighted imaging (SWI)
(A, B, C, D): multiple microhemorrhages mainly
affecting the subcortical white matter, corpus callosum, internal
capsule, and cerebellar peduncles.
Figure 5.
54-year old man with pathological wakefulness after sedation.
Non-confluent multifocal white matter hyperintense
lesions on FLAIR and diffusion, with
variable enhancement. Axial Diffusion (A, B), Apparent
Diffusion Coefficient (ADC) map (C, D), axial postcontrast
FLAIR (E, F), and postcontrast T1 weighted
MR images (G, H). Multiple nodular
hyperintense Diffusion and FLAIR subcortical and corticospinal tracts
lesions, with very mild mass effect on
adjacent structures. The lesions present a
center with an elevation of ADC corresponding to vasogenic
edema and a peripheral ring of reduced ADC corresponding
to cytotoxic edema (C, D). After contrast
administration, small areas of very mild
enhancement are detected (G, H).
Figure 6.
51-year old man with impaired consciousness. Acute necrotizing
encephalopathy. Axial FLAIR (A, C, D), and coronal
FLAIR (B): bilateral FLAIR hyperintensity
(cross) in both thalami (A, B), associated with
involvement of the cerebellar (C), and cerebral (D) white matter
(arrows).
Comparison of patient groups with and without hemorrhagic lesions
The
comparison between patients with and without intracerebral hemorrhagic
lesions shows that the hemorrhagic complications
were more frequently associated with ICU admission
(20/20, 100% versus 12/17, 71%, p=0.01), with acute
respiratory distress syndrome (ARDS) (20/20, 100% versus 11/17, 65%,
p=0.005) and with pathological wakefulness when
sedative therapies were stopped (13/20, 65% versus
2/17, 12%, p=0.002). The time between the onset of
symptoms (most often respiratory) to brain MRI was longer for patients
with intracerebral hemorrhagic lesions (mean
duration of 33 days versus 19 days, p<0.001).
Leukocytosis (median of 13.4 x 109/L versus 10.4 x 109/L,
p=0.03), anemia (median of 87 g/L versus 110 g/L,
p<0.001), and renal dysfunction (urea’s median of 18mmol/L versus
7mmol/L, p=0.026) were more pronounced in the case of
hemorrhagic lesions.
Discussion
Among
the eight groups of brain MRI features classification, three main
neuroradiological patterns appeared more frequently in
patient with severe COVID-19: signal abnormalities
located in the medial temporal lobe, non-confluent multifocal
WM hyperintense lesions on FLAIR and diffusion with variable
enhancement, associated with hemorrhagic lesions, and
extensive and isolated WM microhemorrhages. The presence
of hemorrhage was frequent, and the detection is of clinical importance
as it was associated with worse respiratory,
neurological, and biological status. Nevertheless, the
underlying mechanism of brain abnormalities remains unsolved, and
the direct implication of SARS-CoV-2 is not clear as only one
patient was positive for SARS-CoV-2 RNA in the CSF.
Unilateral
FLAIR and/or diffusion hyperintensities located in medial temporal lobe
were frequent and have been previously reported in one
patient with COVID-19 (10).
The latter is frequently observed in case of infectious
encephalitis (especially with some viruses like Herpes simplex virus,
Human herpesvirus 6, or Epstein-Barr virus) or in
association with autoimmune limbic encephalitis (19).
Non-confluent
multifocal WM hyperintense lesions on FLAIR and diffusion, with
variable enhancement, which could be associated with
hemorrhagic lesions, have rarely been reported in
patients with COVID-19 (20).
The latter presentation is close to what can be observed on brain
MRIs in case of an inflammatory demyelinating disease such as
acute disseminated encephalomyelitis (ADEM) or acute
hemorrhagic leukoencephalitis. However, these two latter
diagnoses cannot only be retained on the radiological presentation
without the typical CSF analysis or clinical
presentation (21,22).
Several putative mechanisms underlying neurological
consequences of COVID-19 are evoked and among them
immunological parainfectious processes (23).
The immunologic assumption is also reinforced by a recent
neuropathological study which described ADEM-like lesions in the
subcortical WM in a patient with severe COVID-19 (24).
Extensive
and isolated WM microhemorrhages pattern was recently described in 7
critically ill patients with COVID-19 (12) and in the neuropathology study above mentioned (24). A similar pattern was recently described in one case (25)
with disseminated intravascular coagulation. However,
according to the criteria endorsed by the International Society on Thrombosis and Haemostasis (27),
when they were available, no case of disseminated
intravascular coagulation was present in our cohort. Its precise
pathophysiology remains uncertain and will require further
studies. Radmanesh et al. (12) evoking the assumptions of hypoxia or small vessel vasculitis.
A small number of patients presented extensive and confluent supratentorial WM FLAIR hyperintensities (figure 2), as previously described by Kandemirli et al. (11) and Radmanesh et al. (12).
Its precise pathophysiology remains unclear: viral
encephalitis (not supported by CSF analysis) or
post-infectious demyelinating diseases, as previously mentioned, may be
evoked. Since most of our patients were admitted to ICUs
for an ARDS, more general assumptions may be
considered, such as delayed post-hypoxic leukoencephalopathy
(27),
metabolic or toxic encephalopathy, and posterior
reversible encephalopathy syndrome (PRES). This last hypothesis is in
accordance with recently published non-hemorrhagic and
hemorrhagic PRES in patients with COVID-19 (28).
Even
if this national neuroimaging cohort remains unique, our study has
several limitations, mainly due to his retrospective
design. The main limitation is that certain laboratory
data were missing for some patients, notably the immunological
tests. Moreover, patients’ outcomes were not always known at the
time of this communication. Thus, the mortality rate is
probably underestimated in our cohort.
In
conclusion, in this multi-institutional study, we report 37 patients
with COVID-19 and abnormal brain MRIs (excluding
ischemic infarcts). Three main neuroradiological
patterns could be distinguished, and the presence of hemorrhage was
associated with worse clinical status. SARS-CoV-2 RNA
was detected in the CSF only in one patient, and the
underlying mechanisms of brain involvement remain unclear. Imaging and
neurological follow up has to be undertaken in order to
evaluate the prognosis of these patients.
By Brian Hoyle
SAN DIEGO, California -- October 18, 2017 -- In the year following
transcatheter aortic valve replacement (TAVR), patients experience an
approximate 20% increased risk of ischaemic stroke and an over 6-fold
increased risk of haemorrhagic stroke compared with patients who
underwent surgical aortic-valve replacement (SAVR), according to results
of a large, nationwide study presented at the 142nd Annual Meeting of
the American Neurological Association (ANA).
The risk of 1-year events was similar for patients undergoing a
coronary-artery bypass graft (CABG) procedure versus percutaneous
coronary intervention (PCI).
“Patient selection may impact this risk,” explained author Laura
Stein, MD, Icahn School of Medicine at Mount Sinai, New York, New York,
at a poster presentation here on October 15.
The risk of stroke following cardiac procedures is reported to be
about 9%; however, this figure is based on a small number of patients,
local rather than national scope, limited types of cardiac procedures,
and a focus on the perioperative period and long-term periods following
surgery.
Dr. Stein and colleagues sought to get a clearer picture of patients’
intermediate risk using data from the 2013 Nationwide Readmission
Database (NRD). The NRD contains readmissions data for over 14 million
insured and uninsured Americans. The team scrutinised the data standard
codes for cardiac procedures, and then analysed relevant data to
determine the risk of stroke for up to 1 year following TAVR vs SAVR,
and CABG vs PCI.
The NRD data included 2,819,649 patients nationwide who had undergone
medical procedure; of these, 653,216 underwent a cardiac procedure,
1,198,209 a non-cardiac procedure, and 968,224 some other medical
procedure. The groups were similar in age, prevalence of obesity, and
length of hospital stay following surgery.
Dr. Stein and colleagues observed that, compared with their
non-cardiac counterparts, patients receiving a cardiac procedure were
more likely to present with atrial fibrillation or flutter, to have
carotid-artery disease, coagulation disorder, congestive heart failure,
coronary-artery disease, and peripheral-artery disease. Those receiving a
cardiac procedure also had a higher prevalence of diabetes,
hypertension, hyperlipidaemia, and renal failure.
The cumulative risk of ischaemic and haemorrhagic stroke was greater
after TAVR compared with SAVR in the unadjusted data as well as
following adjustment for baseline vascular risk factors, hospital bed
size, teaching-hospital status, income, risk of mortality / severity of
illness, and the residence of each subject (urban or rural nationwide).
The fully adjusted data revealed a hazard ratio (HR) for ischaemic
stroke after TAVR, compared with SAVR, of 1.86 (95% confidence interval
[CI]: 1.12 to 3.08) (P = .016). The HR for haemorrhagic stroke comparing
the same procedures was 6.17 (95% CI: 1.97 to 19.33) (P = .0018). There
was no statistically significant difference in the risk of stroke when
CABG was compared with PCI, with a similar 1-year risk of ischaemic
stroke. The risk of haemorrhagic stroke was similar for CABG and PCI
throughout the 1-year follow-up.
The reasons for the increased risk associated with TAVR remain
unknown, the authors concluded, but need to be understood if
interventions are to be developed.
Dr. Stein and colleagues suggested that patients might benefit from
the development of a risk index calculator that would better define the
risk of stroke following cardiac and non-cardiac surgeries.
[Presentation title: Intermediate Risk of Stroke Following Cardiac
Procedures in a Nationally Representative Dataset. Abstract S162]
Is you are on these, how long before your doctor warns you? http://medicalxpress.com/news/2016-11-hemorrhage-statins-drug-combination.html
Two commonly prescribed statins appear to be
associated with a higher risk of bleeding than others when combined
with dabigatran, a drug often used for preventing strokes in patients
with atrial fibrillation, according to a study published today in the Canadian Medical Association Journal.
Hemorrhage, or
bleeding in a critical area or organ, is a possible side effect of
dabigatran (brand name Pradaxa) and occasionally can be severe enough to
warrant hospital admission or emergency department visits.
Cholesterol-lowering statins such as lovastatin and simvastatin may
increase the amount of dabigatran absorbed by the body and thereby
increase the risk of bleeding, something other statins would not be
expected to do.
Researchers conducted two studies on Ontario residents over age 65
who started taking dabigatran between 2012 and 2014. Of the 45,991
patients, 397 experienced a stroke and 1,117 had major hemorrhage. The
risk of bleeding went up by more than 40 per cent in patients taking
lovastatin or simvastatin, compared with those who were given other
statins.
"We found no difference in the risk of stroke in patients receiving
dabigatran who were prescribed lovastatin or simvastatin versus other
statins," said Dr. Tony Antoniou, a pharmacist at St. Michael's Hospital
and researcher in its La Ka Shing Knowledge Institute and an adjunct
scientist at the Institute for Clinical Evaluative Sciences.
"However, an increase in the risk of bleeding requiring hospital
admission or emergency department visits was seen with lovastatin and
simvastatin compared with the other statins," Dr. Antoniou said.
These results suggest that a clinically important drug interaction
exists between dabigatran and both simvasatatin and lovastatin, he said,
and that other statins should be considered instead for patients with
atrial fibrillation, a condition involving an irregular heart rhythm
known as an arrhythmia. According to the Heart and Stroke Foundation of
Canada it is the most common type of arrhythmia, affecting approximately
350,000 Canadians. One of the main complications of atrial fibrillation
is stroke. Individuals with atrial fibrillation have a risk of stroke
that is 3 to 5 times greater than those without atrial fibrillation.
