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.

Saturday, December 13, 2025

The Association Between FT4/FT3 Ratio and Prognosis in Ischemic Stroke: A Retrospective Cohort Study

 Are you that blitheringly stupid you think 'prognosis' gets survivors recovered? Unless there are EXACT PROTOCOLS delivered after the prognosis, it is TOTALLY FUCKING USELESS! No understanding of that is grounds for firing! I take no prisoners in trying to get stroke solve to 100% recovery

The Association Between FT4/FT3 Ratio and Prognosis in Ischemic Stroke: A Retrospective Cohort Study


Affiliations 

Abstract

Background and aim: The FT4/FT3 ratio reflects thyroid hormone metabolism and has emerged as a prognostic marker in cardiovascular diseases. However, its role in ischemic stroke (IS) remains unclear. This study aimed to investigate the association between the FT4/FT3 ratio and 3-month functional outcomes in IS patients.

Methods: We conducted a retrospective cohort study of 199 first-episode IS patients admitted within 14 days of onset between June 2021 and June 2023. Serum thyroid stimulating hormone (TSH), free triiodothyronine (FT3), and free thyroxine (FT4) were evaluated upon admission. Neurological severity was assessed using the National Institutes of Health Stroke Scale (NIHSS) at admission. Functional outcomes were evaluated using the modified Rankin Scale (mRS) at 3 months post-stroke. Poor outcome was defined as an mRS score of 3-5. Separate analyses were conducted according to FT4/FT3 ratio and outcome.

Results: Patients were stratified by median FT4/FT3 ratio (3.75) into low (≤ 3.75, n = 100) and high (> 3.75, n = 99) ratio groups. The high-ratio group had lower FT3 (4.14 ± 0.52 vs. 4.68 ± 0.52 pg/mL, p < 0.001), higher FT4 (17.83 ± 2.10 vs. 15.36 ± 1.69 pmol/L, p < 0.001), more diabetes (52.5% vs. 34%, p = 0.010), and higher proportion of poor outcomes (46.5% vs. 28%, p = 0.007). Receiver operating characteristic (ROC) analysis revealed that the FT4/FT3 ratio demonstrated the highest predictive ability (area under the curve [AUC] = 0.662) with an optimal cut-off of 3.845. After adjusting for NIHSS scores, age, sex, and vascular risks, the FT4/FT3 ratio remained an independent predictor of poor outcomes (odds ratio [OR] = 2.589, 95% confidence interval [CI]: 1.171 - 5.727, p = 0.019). FT4 was a risk factor (OR = 1.324, 95% CI: 1.045 - 1.678, p = 0.020), while FT3 showed a nonsignificant protective trend (OR = 0.551, 95% CI: 0.218 - 1.390, p = 0.207).

Conclusion: An elevated FT4/FT3 ratio may serve as a novel biomarker for predicting poor outcomes in ischemic stroke(Do we now tell patients they are going to have a poor outcome?), reflecting thyroid hormone metabolic dysfunction that potentially exacerbates inflammation and impairs neuronal repair.

Limitations: This study is limited by its small sample size, single-center design, and absence of serial hormone measurements.

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