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Objective: This study aimed to determine the risk factors associated with short-term neurological decline in acute ischemic stroke patients with large vessel occlusion (LVO) who have undergone successful endovascular recanalization through mechanical thrombectomy. Subjects and Methods: We included 168 LVO patients who had successful recanalization in this study. We collected the patients' demographic data and related disease test results. We noted the National Institutes of Health Stroke Scale (NIHSS) scores at the onset and on the 7th day postonset. After comparing the NIHSS scores at these two time points, we analyzed the correlation between the collected data and the NIHSS scores. We selected the logistic regression model variables based on the correlation significance. We included gender, age, diastolic blood pressure, glycosylated hemoglobin, urea nitrogen, hemoglobin, neutrophil-to-lymphocyte ratio (NLR), low-density lipoprotein, and total protein in a logistic regression model. We used the receiver operating characteristic (ROC) curve to evaluate the predictive power of NLR for deterioration. Results: Mechanical thrombectomy significantly lowered the median NIHSS score of LVO patients on the 7th day of onset, while a subset of patients experienced an increased NIHSS score. Correlation analysis revealed significant correlations between the NIHSS score at onset and diastolic pressure, white blood cell count, neutrophil count, creatinine, and urea nitrogen. On the 7th day postonset, NIHSS scores showed significant correlations with glycosylated hemoglobin, white blood cell count, neutrophil count, NLR, red blood cell count, hemoglobin, and urea nitrogen. Logistic regression analysis further revealed that patients with higher NLR are at significantly increased risk of short-term neurological decline. ROC analysis indicated that a higher NLR can serve as a diagnostic marker for potential adverse outcomes of mechanical thrombectomy. Conclusion: While mechanical thrombectomy substantially improves neurological deficits in LVO patients, some patients still experience deterioration. Higher NLR at stroke onset is associated with short-term neurological function decline in acute LVO patients postsuccessful recanalization.

Background: Immunomodulation and cell signaling involve several cytokines, proteins, and other mediators released in response to the trauma, inflammation, or other insults to the central nervous system. This pilot study is part of the registry designed to evaluate the temporal trends among these molecules after an acute ischemic stroke (AIS) in patients. Methods: Twelve AIS patients were enrolled within 24 hours of the symptoms onset. Two sets of plasma samples were collected: First at admission and second at 24 hours after admission. Cytokines/chemokines and other inflammatory molecules were measured using multiplex assay kit. Results: An increased trend in IL-6 (22 vs. 34 pg/ml), IL-8/CXCL8 (87 vs. 98 pg/ml), MMP-9 (16225 vs. 18450 pg/ml), and GMF-ß (999 vs. 3739 pg/ml) levels was observed overtime after an AIS. Patients =60 years had lower levels of plasma MCP-1/CCL2 (50-647 vs. 150-1159 pg/ml), IL-6 (9-25 vs. 20-68 pg/ml), and IL-8 (30-143 vs. 72-630 pg/ml), when compared with patients >60 years old. Conclusion: Cytokines/chemokines and other inflammatory mediators play an important role in the pathogenesis of stroke in addition to mediating poststroke inflammation. Further research is needed to evaluate and characterize the cumulative trends of these mediators for the clinical prognosis or as surrogate biomarkers. [ABSTRACT FROM AUTHOR]

Cardiac arrhythmias occur frequently in patients with acute stroke, with atrial fibrillation (AF) being the most common. Newly detected AF may lead to increased risk of ischemic stroke, which in turn generates stroke recurrence and adverse outcomes. Currently, most studies are focusing on the role of AF in ischemic stroke and attributing cryptogenic ischemic stroke to previously undetected AF. However, in these studies, subjects used to have neither symptoms of palpitation nor evidence of AF. A better understanding of this association will contribute to the management and therapy for patients after clinical decisions regarding stroke patients. Currently, the definition of newly detected AF has not come to an agreement, and the pathophysiology remains incompletely understood, possibly involving complex alterations in both the autonomic network and humoral regulation. Therefore, this review aims to introduce the definition and epidemiology of newly detected AF after stroke with updated information and elucidate the potential pathophysi-ology, such as autonomic imbalance, catecholamine surge, poststroke systematic inflammation, and microvesicles and microRNAs. [ABSTRACT FROM AUTHOR]

Various proteases in the brain contribute to ischemic brain injury. We investigated the involvement of the asparaginyl endopeptidase legumain after experimental stroke. On the basis of gene array studies and in situ hybridizations, we observed an increase of legumain expression in the peri-infarct area of rats after transient occlusion of the middle cerebral artery (MCAO) for 120 mins with a maximum expression at 24 and 48 h. Immunohistochemical analyses revealed the expression of legumain in Iba1+ microglial cells and glial fibrillary acidic protein-positive astrocytes of the peri-infarct area in mice after MCAO. Post-stroke recovery was also studied in aged legumain-deficient mice (45 to 58 weeks old). Legumain-deficient mice did not show any differences in physiologic parameters compared with respective littermates before, during MCAO (45 mins), and the subsequent recovery period of 8 days. Moreover, legumain deficiency had no effect on mortality, infarct volume, and the neurologic deficit determined by the rotating pole test, a standardized grip strength test, and the pole test. However, a reduced number of invading CD74+ cells in the ischemic hemisphere indicates an involvement in post-stroke inflammation. We conclude that legumain is not essential for the functional deficit after MCAO but may be involved in mechanisms of immune cell invasion. [ABSTRACT FROM AUTHOR]

Apolipoprotein E (ApoE), a cholesterol transporter and an immunomodulator, is brain protective after experimental stroke and implicated in brain repair. Here, we study the involvement of ApoE in the restoration of brain function after experimental stroke, by using animal housing conditions that differentially improve recovery after occlusion of the middle cerebral artery occlusion (MCAO). We found that after MCAO the ApoE levels increased in the injured hemisphere over a 30 days recovery period. The exception was a proximal narrow peri-infarct rim, in which ApoE was solely localized in S100β+/glial fibrillary acidic protein (GFAP) negative reactive astrocytes at 4 to 7 days of recovery. Enriched housing after MCAO caused a marked decrease in ApoE levels compared with standard housing conditions, particularly in the ApoE/S100β+ reactive astrocytes. In addition, the levels of interleukin 1β were lower in animals housed in an enriched environment. We propose that during the subacute phase after experimental stroke a zone for tissue reorganization with low cellular ApoE levels is formed. We conclude that the strong sensori-motor stimulation provided by enriched housing conditions mitigates the inflammatory response after stroke decreasing the level of ApoE that may contribute to the observed improvement of functional recovery. [ABSTRACT FROM AUTHOR]