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.

Thursday, October 13, 2022

Post-operative neutrophil-to-lymphocyte ratio and outcome after thrombectomy in acute ischemic stroke

 We don't need more useless prediction of bad outcomes. Do the damn research that prevents those outcomes!

Post-operative neutrophil-to-lymphocyte ratio and outcome after thrombectomy in acute ischemic stroke

Shen-Jie Li1, Shan-Shan Cao1, Pei-Sheng Huang1, Xin Nie2, Yang Fu1 and Jian-Ren Liu1*
  • 1Department of Neurology, Stroke Center, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China
  • 2Biostatistics Office of Clinical Research Unit, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China

Background: Neutrophil to lymphocyte ratio (NLR) is a novel inflammatory marker to predict adverse cardiovascular events. However, there is a lack of data on hemorrhagic transformation (HT) and neurological outcome after mechanical thrombectomy in acute ischemic stroke (AIS). We investigated whether NLR before and after thrombectomy for patients with AIS was associated with HT and neurological outcomes.

Methods: We performed a retrospective analysis of consecutive patients with anterior circulation AIS who underwent thrombectomy. HT was evaluated by CT within 24 h after thrombectomy. Clinical data had been collected retrospectively; laboratory data were extracted from our electronic hospital information system. NLR was obtained at admission (NLR1) and immediately after thrombectomy (NLR2). The main outcomes were post-interventional intracranial hemorrhage and unfavorable functional status (modified Rankin scale scores of 3–6) 3 months post-stroke.

Results: A total of 258 patients with AIS, according to the NIHSS (median 14), were included. NLR2 was higher in patients who developed HT after thrombectomy and unfavorable neurological outcomes 3 months post-stroke (p < 0.001) than in those without HT or favorable outcomes, even after correction for co-factors [Odds Ratio (OR) 1.35 for HT, 95% confidence interval (CI)1.16–1.57, p < 0.001, and 1.85 for unfavorable outcome, 95%CI 1.57–2.17, p < 0.001]. The optimal cutoff value for the NLR2 as an indicator for auxiliary diagnosis of HT and the unfavorable outcome was 8.4 and 8.8, respectively.

Conclusion: NLR immediately after thrombectomy is a readily available biomarker of HT and neurological outcomes in patients with AIS.

Introduction

Acute ischemic stroke (AIS) is a common disease that affects elderly people (1). A randomized controlled trial confirms the improved reperfusion, early neurologic recovery, and functional outcome of thrombectomy compared to intravenous thrombolysis (IVT) (2). However, hemorrhagic transformation (HT) is a secondary intracranial hemorrhage after thrombectomy, with an incidence of about 10%. It is a major complication of thrombectomy and AIS in the acute phase (3), which often indicates a poor prognosis (4). Therefore, to improve the effectiveness of thrombectomy in clinical practice, it is of great significance to identify the risk factors of HT after thrombectomy.

Inflammation and immune responses run through all stages of cerebral ischemia and stroke progression, and when an ischemic stroke occurs, brain tissue releases pro-inflammatory chemokines, triggering strong inflammatory responses (5). Ischemic stroke reperfusion occurs after an endovascular procedure, and the damaged tissue is reoxygenated (6), resulting in the accelerated production of reactive oxygen species (ROS) and reactive nitrogen species. Inflammation caused by increased free radicals triggers the accumulation of inflammatory cells in the ischemic area. Interactions between endothelial cells and inflammatory cells lead to the release of many cytokines and amplify ischemic injury through reperfusion. Circulating neutrophils enter injured brain regions shortly after ischemia and then participate in disrupting the blood–brain barrier (BBB) and increasing tissue damage (7, 8). The greater the number of neutrophils, the greater the enhancement of tissue damage, as they lead to the release of inflammatory mediators, ROS, and various proteolytic enzymes. Lymphopenia may reflect cortisol-related stress responses and sympathetic tone (9), which may increase pro-inflammatory cytokine production (10). NLR as a reflection of innate (neutrophil) and adaptive (lymphocyte) immune responses has been extensively studied to assess the severity of inflammation associated with systemic or local diseases. Compared with a single index, a comprehensive index has higher validity and specificity. An increased NLR level with neutrophil exaltation and lymphocyte depletion suggests an imbalance in the interplay between central and peripheral inflammation induced by stroke.

However, previous studies focused on higher preoperative NLR levels as an independent predictor of symptomatic intracerebral hemorrhage (sICH) after thrombectomy (11). Stroke-related inflammation may be more closely related to HT after thrombectomy and functional status 3 months post-stroke, and NLR can be more accurately assessed in early follow-up after thrombectomy.

In the present study, we sought to investigate the association of NLR levels immediately after thrombectomy with thrombectomy-related HT and neurological outcomes in patients with AIS.

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