Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective 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.

Monday, October 8, 2012

Secondary stroke prevention: misguided by guidelines?

This is a good test to find out if your doctor/clinic/hospital follows research at all.
Do they know about this? Its only 2 months old.
 http://www.ncbi.nlm.nih.gov/pubmed/22997997?dopt=Abstract
 Acta Cardiol. 2012 Aug;67(4):431-8.

Abstract

OBJECTIVES:

Despite large clinical trials, there is no consensus about the best antithrombotic strategy for the secondary prevention of non-cardioembolic ischaemic stroke.This retrospective study is the first to combine the results of the most important trials and to integrate data on study validity, effectiveness, adverse events, risk of non-compliance, and cost.

METHODS:

We searched MEDLINE, EMBASE, and the Cochrane Database (1996 to July 2011) and selected long-term secondary prevention trials with treatment with aspirin, dipyridamole, clopidogrel, aspirin plus dipyridamole, or aspirin plus clopidogrel. Subgroup analyses were included to explain differences in interpretations that could have led to the differences in guidelines.

RESULTS:

Two trials showed a small but significant reduction with aspirin plus dipyridamole compared to aspirin (ARR 1.5%, P < 0.05 and ARR 1.0%, P < 0.05). There was no effect on vascular death. One trial showed a small but statistical significant reduction with clopidogrel compared to aspirin (ARR 0.5%, P < 0.05). The association of clopidogrel with aspirin could not show any significant benefit compared to clopidogrel monotherapy, nor compared to aspirin monotherapy, but showed higher rates of adverse events. Significantly more patients discontinued treatment with aspirin plus dipyridamole compared to aspirin monotherapy (34.5% versus 13.4% and 29.0% versus 22.2%, P < 0.001) and clopidogrel monotherapy (29.1% versus 22.6%, P < 0.001). Transposition of statistical significant reductions in stroke recurrence into clinical significance could not be supported.

CONCLUSIONS:

Despite changes in international guidelines, aspirin monotherapy should retain its position as the main antiplatelet agent for secondary prevention of non-cardioembolic ischaemic stroke.

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