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, September 29, 2025

Elevated systemic immune-inflammation index is associated with stroke-associated pneumonia in acute ischemic stroke: a retrospective cohort study

Fuck, we don't need predictions of pneumonia you blithering idiots, solve the problem of preventing that pneumonia in the first place.  I'd have you all fired.

You've known about this problem for a long time. GET THERE! 

Just maybe this vaccine!

Pneumonia Vaccine (3 posts to July 2020)

11% Stroke-associated pneumonia (2 posts to October 2020)

 Elevated systemic immune-inflammation index is associated with stroke-associated pneumonia in acute ischemic stroke: a retrospective cohort study


Tingting DuanTingting Duan1Ming YangMing Yang1Yiming Zhang&#x;Yiming Zhang2Chunyan Zhu&#x;Chunyan Zhu2Zichen Rao
&#x;Zichen Rao2*
  • 1Department of Neurology, The Quzhou Affiliated Hospital of Wenzhou Medical University, Quzhou People’s Hospital, Quzhou, Zhejiang, China
  • 2Department of Endocrinology, The Quzhou Affiliated Hospital of Wenzhou Medical University, Quzhou People’s Hospital, Quzhou, Zhejiang, China

Stroke-associated pneumonia (SAP) is a frequent complication of acute ischemic stroke (AIS) that contributes to poor clinical outcomes. The systemic immune-inflammation index (SII), derived from neutrophil, lymphocyte, and platelet counts, may reflect post-stroke immune imbalance, but its role in predicting SAP remains unclear. In this retrospective study, we analyzed 1,767 AIS patients and evaluated the association between log₂-transformed SII and the occurrence of SAP using multivariable logistic regression, generalized additive models, and two-piecewise regression. SAP developed in 21.3% of patients during hospitalization. Higher SII levels were independently associated with increased SAP risk after adjustment for age, sex, vascular risk factors, comorbidities, baseline National Institutes of Health Stroke Scale (NIHSS) score, and dysphagia assessed by Kubota Water Drinking Test (KWDT). Patients in the highest SII quartile had a significantly greater likelihood of developing SAP compared to those in the lowest quartile (adjusted odds ratio = 2.03, 95% confidence interval: 1.21–3.38, p = 0.0069). A non-linear, threshold-dependent relationship was identified, with SAP risk increasing substantially beyond log₂-SII ≈ 8.5. Receiver operating characteristic (ROC) analysis demonstrated moderate predictive performance of SII for SAP (area under the curve (AUC) = 0.726), while C-reactive protein (CRP) showed superior discrimination (AUC = 0.826 p < 0.0001). Supplementary sensitivity analyses, including a fully adjusted model without NIHSS and KWDT and an alternative model replacing these with the A2DS2 score (Age, Atrial fibrillation, Dysphagia, Sex, Stroke Severity), showed consistent results, supporting the robustness of our findings. These findings suggest that SII may serve as a cost-effective and accessible biomarker to aid early identification of high-risk AIS patients.

Introduction

Stroke remains one of the leading causes of mortality and long-term disability worldwide, with acute ischemic stroke (AIS) accounting for approximately 80% of all cases (1). Despite advances in acute stroke management, complications during hospitalization, particularly stroke-associated pneumonia (SAP), continue to pose significant challenges (2). SAP occurs in 10 to 30% of AIS patients and is closely associated with prolonged hospital stays, increased healthcare costs, and worse functional outcomes, including higher mortality rates (3). Early identification of high-risk patients is essential to guide preventative interventions and improve prognosis (4).

Emerging evidence suggests that systemic inflammation plays a pivotal role in the development of SAP by disrupting immune homeostasis and enhancing susceptibility to pulmonary infections following AIS (5). Conventional inflammatory biomarkers such as CRP, white blood cell (WBC) count, and neutrophil-to-lymphocyte ratio (NLR) have been widely used to assess systemic inflammation; however, their predictive accuracy for SAP remains suboptimal (6). The systemic immune-inflammation index (SII) calculated from platelet count, neutrophil count, and lymphocyte count, is a novel composite marker that reflects the balance between pro-inflammatory and immune-regulatory responses (7). Recent studies have demonstrated its prognostic value in various cardiovascular and oncologic conditions, but its predictive utility in SAP remains underexplored (8). In this study, we focused on SII as a comprehensive marker of immune-inflammatory balance, and compared it with CRP, a widely used reference biomarker in stroke research, to assess whether SII provides additional or complementary prognostic value beyond CRP. Moreover, existing studies evaluating inflammatory markers in SAP have primarily focused on linear relationships, potentially overlooking complex non-linear and threshold effects (9). For example, Kuang et al. (10) examined the association between SII and SAP risk in a smaller, mixed cohort of acute stroke patients and reported a linear relationship, without investigating potential non-linear patterns or thresholds. Whether elevated SII levels exhibit a dose–response relationship or specific thresholds beyond which SAP risk dramatically increases has not been fully elucidated. Addressing these knowledge gaps is critical for refining clinical risk stratification and informing targeted preventative strategies (11).

We posited that early elevation of the SII, as a marker of post-stroke immune disequilibrium, would identify AIS patients at independently higher risk of SAP, and that the exposure–response might be non-linear with a clinically relevant threshold. To test this hypothesis, we investigated the association between SII and the development of SAP in patients with AIS by analyzing a large, retrospective cohort. Specifically, we examined the predictive value of log₂-transformed SII, explored potential non-linear and threshold effects through advanced modeling approaches, and compared the diagnostic performance of SII with established inflammatory biomarkers such as CRP.

More at link.

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