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.

Friday, December 22, 2023

Inflammatory Biomarkers and Stroke Subtype

Didn't your competent? stroke doctor start using colchicine and canakinumab years ago? Or don't you have functioning stroke doctor? I'd run away from such incompetence!

AHA: Colchicine Prevents Postop Afib December 2011 

Could Old Gout Drug Offer New CV Benefits? November 2015 

Anti-inflammatory therapy for preventing stroke and other vascular events after ischaemic stroke or transient ischaemic attack November 2017

The latest here:

Inflammatory Biomarkers and Stroke Subtype

Seemant Chaturvedi, MD https://orcid.org/0000-0001-8660-7644, and Gian Marco De Marchis https://orcid.org/0000-0002-0342-9780Authors Info & Affiliations
January 23, 2024 issue
102 (2)
https://doi.org/10.1212/WNL.0000000000208098
 Abstract

    • Abstract

    Inflammation is an established pathway in the formation, growth, and rupture of atherosclerotic plaques. Inflammation is thus essential to the pathogenesis of coronary heart disease and some types of ischemic stroke.1 The benefit of anti-inflammatory therapies, such as colchicine2 and the anti-IL1β canakinumab,3 is proven in patients with coronary heart disease, yet it remains unproven for patients with ischemic stroke. Compared with coronary heart disease, the etiology of stroke is more heterogeneous. Besides arterio-arterial atherogenic embolism, possible etiologies are penetrator artery occlusion, cardioembolism, and other mechanisms. Finding a stroke etiology remains elusive in up to 30%–40% of patients despite a full evaluation. Understanding whether the stroke etiology modifies the association between inflammatory markers and recurrence risk is an important step to improve selection of patients for randomized trials on anti-inflammatory agents. IL-6 and high-sensitive CRP (hs-CRP) have been implicated in a higher recurrence risk after ischemic stroke by both an individual participant data meta-analysis4 and a Mendelian randomization study,5 but granular, in vivo results stratified by stroke etiology are lacking.

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