I wonder about the contraindication of tPA use in the last 3 months? I know I wasn't asked if I was taking aspirin or anything else.
Whom is going to decide if this is enough information to change the
stroke protocol on this use? And then disseminate this to all stroke
doctors, emergency rooms and stroke hospitals?
WHO IS GOING TO DO THIS?
Our fucking failures of stroke associations obviously will not take on
this challenge. You as a stroke patient are simply screwed. YOU will need to remember this and notify your emergency room doctors.
http://medicalresearch.com/stroke/benefits-of-tps-outweigh-risks-in-ischemia-stroke-even-in-patients-on-antiplatelet-medications/19164/
MedicalResearch.com Interview with:
Ying Xian, PhD
Assistant Professor of Medicine.
Member in the Duke Clinical Research Institute
Medical Research: What is the background for this study? What are the main findings?
Dr. Xian: Intravenous
tissue plasminogen activator (tPA) is the only FDA approved medical
therapy to reduce disability and improve outcomes for patients with
acute ischemic stroke. But treatment with tPA also carries the risk of
symptomatic intracranial hemorrhage (sICH), which is often fatal. Nearly
half of ischemic stroke patients are taking antiplatelet drugs such as
aspirin and/or clopidogrel prior to stroke. We found these patients had
higher risk for sICH when treated with tPA. But the risk is relatively
small. For every 147 patients on aspirin treated with tPA, only 1 more
symptomatic intracranial hemorrhage as compared with those treated with tPA
without prior antiplatelet therapy. The risk is slightly higher among
those on dual antiplatelet therapy of aspirin and clopidogrel (number
needed to harm 60). Despite the higher bleeding risk, patients treated
with tPA on prior antiplatelet therapy appeared to have better
functional outcomes in terms of ambulatory status and modified Rankin
scale than those not on prior antiplatelet therapy. Therefore, overall
the benefits of thrombolytic therapy may outweigh the risks.
Medical Research: What should clinicians and patients take away from your report?
Dr. Xian: Considering intravenous tPA
is the only FDA approved medical therapy and remains substantially
underused worldwide for patients with acute ischemic stroke, clinicians
should consider intravenous tPA for eligible patients on prior
antiplatelet therapy. I would like to quote from Dr. Mark Alberts, Vice
Chair of Clinical Affairs in the Department of Neurology and
Neurotherapeutics at UT Southwestern Medical Center, “the real risk is
not treating.”
Medical Research: What recommendations do you have for future research as a result of this study?
Dr. Xian: As more potent P2Y12 inhibitors such as prasugrel
and ticagrelor are increasingly used in the Unites States, future
research is needed provide guidance on tPA for patients who developed
ischemic stroke while taking these new antiplatelet drugs.
Citation:
Australian researchers have come up with a non-invasive ultrasound
technology that clears the brain of neurotoxic amyloid plaques -
structures that are responsible for memory loss and a decline in
cognitive function in Alzheimer’s patients.
If a person has Alzheimer’s disease, it’s usually the result of a
build-up of two types of lesions - amyloid plaques, and neurofibrillary
tangles. Amyloid plaques
sit between the neurons and end up as dense clusters of beta-amyloid
molecules, a sticky type of protein that clumps together and forms
plaques.
Neurofibrillary tangles
are found inside the neurons of the brain, and they’re caused by
defective tau proteins that clump up into a thick, insoluble mass. This
causes tiny filaments called microtubules to get all twisted, which
disrupts the transportation of essential materials such as nutrients and
organelles along them, just like when you twist up the vacuum cleaner
tube.
As we don’t have any kind of vaccine or preventative measure for
Alzheimer’s - a disease that affects 343,000 people in Australia, and 50
million worldwide - it’s been a race to figure out how best to treat
it, starting with how to clear the build-up of defective beta-amyloid
and tau proteins from a patient’s brain. Now a team from the Queensland
Brain Institute (QBI) at the University of Queensland have come up with a
pretty promising solution for removing the former.
Publishing in Science Translational Medicine,
the team describes the technique as using a particular type of
ultrasound called a focused therapeutic ultrasound, which non-invasively
beams sound waves into the brain tissue. By oscillating super-fast,
these sound waves are able to gently open up the blood-brain barrier,
which is a layer that protects the brain against bacteria, and stimulate
the brain’s microglial cells to activate. Microglila cells are
basically waste-removal cells, so they’re able to clear out the toxic
beta-amyloid clumps that are responsible for the worst symptoms of
Alzheimer’s.
The team reports fully restoring the memory function of 75 percent
of the mice they tested it on, with zero damage to the surrounding
brain tissue. They found that the treated mice displayed improved
performance in three memory tasks - a maze, a test to get them to
recognise new objects, and one to get them to remember the places they
should avoid.
"We’re extremely excited by this innovation of treating
Alzheimer’s without using drug therapeutics," one of the team, Jürgen
Götz, said in a press release.
"The word ‘breakthrough’ is often misused, but in this case I think
this really does fundamentally change our understanding of how to treat
this disease, and I foresee a great future for this approach."
The team says they’re planning on starting trials with higher
animal models, such as sheep, and hope to get their human trials
underway in 2017.
You can hear an ABC radio interview with the team here.