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.

Sunday, February 7, 2021

EXPRESS: Inflammatory cytokines, high sensitivity CRP, and risk of 1-year vascular events, death and poor functional outcome after stroke and TIA

 Maybe something is some of these? WHOM do we ask to do followup research? Since there is NO STROKE LEADERSHIP nothing will occur.

Sabinsa’s curcuminoid improves cytokine levels in traumatic brain injury patients

 July 2020 

Candesartan could ameliorate the COVID-19 cytokine storm

 August 2020

Spices in a high-saturated-fat, high-carbohydrate meal reduce postprandial proinflammatory cytokine secretion in men with overweight or obesity: A 3-period, crossover, randomized controlled trial March 2020 

Cannabinoids, Blood–Brain Barrier, and Brain Disposition March 2020 

In here is this line: Several findings indicate that CBD can modify the deleterious effects on BBB caused by inflammatory cytokines

Positive affect and markers of inflammation: Discrete positive emotions predict lower levels of inflammatory cytokines. May 2015 

Researchers Discover New Way to Block Inflammation in Alzheimer’s, Atherosclerosis and Type-2 Diabetes July 2013

 

The latest here:

EXPRESS: Inflammatory cytokines, high sensitivity CRP, and risk of 1-year vascular events, death and poor functional outcome after stroke and TIA

First Published February 4, 2021 Research Article 

Background

Inflammation driven by pro-inflammatory cytokines is a new therapeutic target in coronary disease. Few data exist on the association of key upstream cytokines and post-stroke recurrence. In a prospective cohort study, we investigated the association between pivotal cytokines, CRP and 1-year outcomes.

Methods

BIO-STROKETIA is a multi-centre prospective cohort study of non-severe ischemic stroke (mRS≤3) and TIA. Controls were patients with transient symptoms attending TIA clinics with non-ischemic final diagnosis. Exclusion criteria were severe stroke, infection and other pro-inflammatory disease. High-sensitivity serum C-reactive protein (CRP) and cytokines (interleukin [IL] 6, IL-1β, IL-8, IL-10, IL-12, interferon-γ [IFN-γ], tumor-necrosis factor-α [TNF-α]) were measured. The primary outcome was 1-year recurrent stroke/coronary events (fatal and non-fatal).

Results

680 patients (439 stroke, 241 TIA) and 68 controls were included. IL-6, IL-1β, IL-8, IFN-γ, TNF-α, and CRP were higher in stroke/TIA cases (p≤0.01 for all). On multivariable Cox regression, IL-6, IL-8, and CRP independently predicted 1-year recurrent vascular events (adjusted HRs [aHR] per-quartile increase IL-6 1.31,CI 1.02-1.68, p=0.03; IL-8 1.47, CI 1.15-1.89, p=0.002; CRP 1.28 CI, 1.01-1.62, p=0.04). IL-6 (aHR 1.98, CI 1.26-3.14, p=0.003) and CRP (aHR 1.81, CI 1.20-2.74, p=0.005) independently predicted 1-year fatality. IL-6 and CRP (adjusted OR per-unit increase 1.02, CI 1.01-1.04) predicted poor functional outcome, with a trend for IL-1 (p=0.054).

Conclusion

Baseline inflammatory cytokines independently predicted late recurrence, supporting a rationale for randomised trials of anti-inflammatory agents for prevention after stroke and suggesting that targeted therapy to high-risk patients with high baseline inflammation may be beneficial.(How do we change may to will? With NO STROKE LEADERSHIP nothing will be done.)

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