Super Formula for Soluble C-Type Lectin-Like Receptor 2 × D-Dimer in Patients With Acute Cerebral Infarction.

Acute cerebral infarction (ACI) includes atherosclerotic and cardiogenic ACI and involves a thrombotic state, requiring antithrombotic treatment. However, the thrombotic state in ACI cannot be evaluated using routine hemostatic examinations. Plasma soluble C-type lectin-like receptor 2 (sCLEC-2) and D-dimer levels were measured in patients with ACI. Plasma sCLEC-2 and D-dimer levels were significantly higher in patients with ACI than in those without it. The sCLEC-2 × D-dimer formula was significantly higher in patients with ACI than in those without it. A receiver operating characteristic curve showed a high sensitivity, area under the curve, and odds for diagnosing ACI in the sCLEC-2 × D-dimer formula. Although the sCLEC-2 and D-dimer levels were useful for the differential diagnosis between cardiogenic and atherosclerotic ACI, the sCLEC-2 × D-dimer formula was not useful. sCLEC2 and D-dimer levels are useful for the diagnosis of ACI and the sCLEC2 × D-dimer formula can enhance the diagnostic ability of ACI, and sCLEC2 and D-dimer levels may be useful for differentiating between atherosclerotic and cardioembolic ACI.

Prognostic Significance of Asymptomatic Cerebral Infarction in Patients After Cardiac Catheterization.

Recent studies have showed that asymptomatic cerebral infarction (ACI) developed in a reasonable number of patients after cardiac catheterization. However, no study has investigated the long-term prognostic impact of ACI after cardiac catheterization. We investigated whether ACI after cardiac catheterization affects long-term mortality and subsequent cardiovascular events.We retrospectively enrolled patients who underwent cardiac catheterization before cardiac surgery and cerebral diffusion-weighted magnetic resonance imaging (DWI). The incidence and clinical features of ACI were investigated. The long-term prognosis, including all-cause mortality and subsequent major cardiovascular events (MACE; all-cause mortality, stroke, acute myocardial infarction, fatal arrhythmia, and hospitalized heart failure), was also assessed.A total of 203 patients were enrolled. Of these, 10.3% had ACI diagnosed by DWI. There were no differences in baseline characteristics between patients with and without ACI, except more frequent history of symptomatic stroke in patients with ACI. In the Kaplan-Meier analysis during a median follow-up of 1009 days, the patients with ACI showed worse mortality and a slightly higher occurrence of MACE compared with those without ACI (P = 0.01 and P = 0.08, respectively). In addition, ACI was a prognostic marker independent of age, surgery type, and history of stroke.ACI after cardiac catheterization frequently developed and was also associated with long-term prognosis. It may be an independent prognostic marker in high-risk patients who underwent subsequent cardiac surgery.

Development of a model for predicting acute cerebral infarction induced by non-variceal upper gastrointestinal bleeding.

OBJECTIVE: To evaluate the risk factors for acute cerebral infarction(ACI) in patients with non-variceal upper gastrointestinal bleeding(NVUGIB), and construct a model for predicting ACI in NVUGIB patients. METHODS: A model for predicting ACI induced by NVUGIB was established on the basis of a retrospective study that involved 1282 patients who were diagnosed with NVUGIB in the emergency department and Gastroenterology Department of Nanchang University Affiliated Ganzhou Hospital from January 2019 to December 2021. Receiver operating characteristic (ROC) curves were drawn to evaluate the sensitivity and specificity of the model and CHA2DS2-VASc score to predict ACI. Delong's test was used to compare AUCs of the present score and the CHA2DS2-VASc score. RESULTS: There were 1282 patients enrolled in the study, including 69 in the ACI group and 1213 in the non-ACI group. Multivariate analysis revealed that hypertension, diabetes, red blood cell (RBC) transfusion, mechanical ventilation, D-dimer, rate pressure product (RPP), somatostatin and mean platelet volume (MPV) were factors associated with ACI induced by NVUGIB. A model based on the eight factors was established, Logit(P)= 0.265 + 1.382 × 1 + 1.120 × 2 + 1.769 × 3 + 0.839 × 4-1.549 × 5-0.361 × 6 + 0.045 × 7 + 1.158 × 8(or 1.069 ×9) (X1, hypertension=1; X2, diabetes=1; X3, RBC transfusion=1; X4, mechanical ventilation=1; X5, somatostatin=1; X6, MPV(fL); X7, D-dimer(ng/l); X8, low RPP= 1; X9, high RPP = 2). The area under ROC curve of the model was 0.873, the sensitivity and specificity were 0.768 and 0.887, respectively. The area under ROC curve of CHA2DS2-VASc score was 0.792, the sensitivity and specificity were 0.728 and 0.716, respectively. Delong's test showed the area under ROC curve of the present study was significantly larger than that of CHA2DS2-VASc score. CONCLUSIONS: Hypertension, diabetes, RBC transfusion, mechanical ventilation, D-dimer, RPP, somatostatin and MPV were factors associated with ACI induced by NVUGIB. A model constructed based on these factors showed excellent prediction of ACI, and was superior to CHA2DS2-VASc score. However, this needs to be further validated by multi-center study with a larger sample size.

Dysregulation of Serum UCA1 and Its Clinical Significance in Patients with Acute Cerebral Infarction.

OBJECTIVE: To investigate the expression of lncRNA UCA1 in serum of patients with acute cerebral infarction (ACI) and its relationship with prognosis. METHODS: The serum lncRNA UCA1 level in participants was detected, and the correlation between the neurological function score (NIHSS score) of ACI patients and lncRNA UCA1 expression was analyzed. Patients were followed up at 3 months after discharge and were divided into favorable and unfavorable prognostic groups according to the modified Rankin scale (mRs). The risk factors of ACI patients with poor prognosis were analyzed, and the predictive value of each index for ACI prognosis was evaluated by ROC curve. RESULTS: The level of lncRNA UCA1 in ACI group was increased (P<0.001). ROC analysis showed that high lncRNA UCA1 expression had clinical significance for the diagnosis of ACI. Spearman correlation analysis revealed that NIHSS score was positively correlated with lncRNA UCA1 expression level in ACI group (r=0.6537, P<0.001). Hcy level and NIHSS score in poor prognosis group (n=63) were higher than those in good prognosis group (n=84), and lncRNA UCA1 level in serum in poor prognosis group was increased in comparison to good prognosis group (P<0.05). Logistic regression analysis investigated that admission NIHSS score, infarct size, and increased lncRNA UCA1 were the risk factors affecting the prognosis of ACI. CONCLUSION: Serum lncRNA UCA1 is abnormally elevated in ACI patients, and the elevated lncRNA UCA1 not only shows high accuracy in the diagnosis of ACI, but also has a certain predictive value for poor prognosis of ACI.

Silent Cerebral Infarcts in Iraqi Patients with Sickle Cell Disease.

Silent ischemic infarcts have been reported to be the most frequent neurological abnormalities in sickle cell disease (SCD) in several studies worldwide. However, no previous studies investigated this neurological disorder in Iraqi SCD patients. To address this issue, a total of 52 patients with a median age of 20 years (range 10-46) and including 46.2% males were enrolled. Patients were clinically evaluated and their records were reviewed. They had full blood and reticulocyte counts, hemoglobin F estimation, serum lactic dehydrogenase and bilirubin assayed, as well as brain magnetic resonance imaging (MRI) to screen for silent cerebral infarcts. Six out of the 52 patients (11.5%) had silent cerebral infarcts, all of which were in the deep white matter, ranging from 6 to 10 mm in their largest diameters. There were no significant differences in age, sex, or sickle cell genotype between those with silent cerebral infarcts and those without it. Those with silent cerebral infarcts had lower median hemoglobin, higher reticulocytes and lower pain frequencies than those without it, yet again this was not significant. Follow up MRI in four out of the six silent infarct patients showed no additional lesions and no increase in size of the original ones after six to eight months. In conclusion, it appears that the frequency of silent cerebral infarcts in Iraqi SCD patients is lower than the bulk of the literature from other populations. Further studies to screen for genetic polymorphisms that may explain this lower rate may be informative.

Predictive value of P wave parameters, indices, and a novel electrocardiographic marker for silent cerebral infarction and future cerebrovascular events.

BACKGROUND: Silent cerebral infarction (SCI) is a neuronal injury without a clinically apparent stroke or transient ischaemic attack. Left atrial cardiomyopathy is closely associated with SCI. P wave changes in the electrocardiogram (ECG) provide significant information about the development of atrial cardiomyopathy. This study evaluated the role of P wave parameters and indices and a novel ECG parameter in predicting SCI, future cerebrovascular events, and atrial fibrillation/flutter. MATERIALS AND METHODS: A total of 272 patients were retrospectively screened and divided into two groups according to SCI. Cerebrovascular events and atrial fibrillation/flutter were defined as the study's outcomes. P wave parameters, indices, and a novel ECG parameter called the P wave ratio (PWR) were calculated from ECGs, and the relationship between SCI and outcomes was investigated. RESULTS: The maximum P wave duration (PWD), P wave dispersion (PWdisp), PWD measured from the D2 lead (PWDD2), P wave peak time measured from the D2 lead (PWPTD2), PWPT measured from the V1 lead (PWPTV1), and P wave terminal force (PWTFV1) were significantly longer in the SCI group. Both partial and advanced inter atrial block (IAB) were significantly high in the SCI group. The novel parameter P wave ratio (PWR) was significantly longer in the SCI group (0.55 ± 0.08 vs. 0.46 ± 0.09; p < 0.001). In multivariate regression analysis, PWdisp (OR: 1.101, p < 0.001), PWPTD2 (OR: 1.095, p = 0.017), and PWR (OR: 1.231, p < 0.001) were found to be independent predictors of SCI. Cox regression analysis revealed that the PWR (HR 1.077; 95% CI 1.029-1.128; p = 0.001) was associated with cerebrovascular events and atrial fibrillation/flutter. CONCLUSION: In our study, we observed that PWR could be a valuable parameter for predicting SCI and future cerebrovascular events.

Hyperacute synchronous cardiocerebral infarction in a patient with new-onset atrial fibrillation: a case of myocardial infarction with nonobstructive coronary arteries.

Hyperacute synchronous cardiocerebral infarction (CCI) is an extremely rare condition with an incidence of 0.009%. In the acute stage of ischemic stroke, there is a high prevalence of ECG abnormalities. Prolonged QTc, atrial fibrillation (AF) and ECG changes indicative of ischemic heart disease, such as Q waves, ST depression, and T wave inversion, were the most prevalent changes. There are three types of simultaneous CCI: cardiac conditions that cause cerebral infarction, cerebral infarction caused by cardiac conditions, and (c) dysregulation of the brain-heart axis or cerebral infarction causing myocardial infarction. Herein, we present a case of hyperacute synchronous CCI in an elderly patient with new-onset AF and myocardial infarction with nonobstructive coronary arteries (MINOCA).

The value of serum Lp-PLA2 combined with MPO in the diagnosis of cerebral infarction caused by large artery atherosclerosis.

OBJECTIVE: To explore the value of serum lipoprotein-associated phospholipase A2（Lp-PLA2）combined with myeloperoxidase（MPO）for the diagnosis of large artery atherosclerosis(LAA) cerebral infarction. METHODS: Baseline data were collected from patients with first-ever acute cerebral infarction, serum Lp-PLA2 and MPO levels were measured. The etiology of cerebral infarction was classified according to the Chinese Ischemic Stroke Subtype Classification Standard. The risk factors associated with LAA cerebral infarction were identified by univariate and multivariate regression analysis. The diagnostic value of serum Lp-PLA2 and MPO for LAA cerebral infarction was assessed by the area under the receiver-operating characteristic (ROC) curve. RESULTS: Overall 368 patients were involved, 148 patients (40.22 %) were LAA. The serum La-PLA2 and MPO levels were higher in the LAA group than those in non-LAA group (23.06 ± 3.39 ng/mL versus 17.48 ± 3.26 ng/mL; 93.60 ± 9.58 ng/mL versus 75.98 ± 15.53 ng/mL; P < 0.001 for both). Multivariate analysis showed that elevated levels of serum Lp-PLA2 (OR 1.742, 95 %CI 1.499-2.025; P < 0.001) and MPO (OR 1.060, 95 % CI 1.026-1.096; P = 0.001) were the independent risk factors of LAA cerebral infarction. The area under curve of the serum Lp-PLA2 combined with MPO for the diagnosis of LAA cerebral infarction was 0.896 [0.866 ∼ 0.927] (P < 0.001). CONCLUSION: Serum Lp-PLA2 combined with MPO could be valued as a predictor of acute cerebral infarction caused by large artery atherosclerosis.

Effects of comprehensive care measures based on the HAPA model on self-care, neurotransmitters and clinical outcomes in cerebral infarction patients.

OBJECTIVE: Cerebral infarction is induced by cerebral artery occlusion, resulting in ischemia, hypoxia, necrosis of brain cells in the corresponding blood supply area, and then dysfunction. Health action process approach (HAPA) model emphasizes the proposal and practice of health behavior as a whole and uses self-monitoring and encouraging ultimately developed health behavior. The present study explores the effects of comprehensive nursing measures of HAPA model on neurotransmitters, self-care ability and clinical outcomes of cerebral infarction patients. PATIENTS AND METHODS: One hundred and ten patients with cerebral infarction diagnosed and treated in our hospital from July 2020 to February 2022 were included as the subjects. The subjects were randomly grouped as the control (55 patients) and the study group (55 patients) and received conventional nursing measures and additional comprehensive nursing measures of HAPA model, respectively. The patients were tested for changes in self-care ability, nerve damage [myelin basic protein (MBP), S100B, glial fibrillary acidic protein (GFAP), neuron-specific enolase (NSE)] and neurotransmitter indexes [acid-soluble protein (Asp), neuropeptide Y (NPY), substance P (SP), glutamate (Glu)], respectively. The patients were considered as the good prognosis group (47 cases) and poor prognosis group (63 cases) according to the prognosis after comprehensive care. The logistic regression model was used to analyze the risk factors affecting the poor prognosis of patients with cerebral infarction. RESULTS: After nursing, China Stroke Scale (CSS) score, the Fugl Meyer Rating Scale (FMA) score and Barthel index were significantly higher in both groups than before nursing, and all indexes were significantly higher in the study group than in the control group (p< 0.05). The length of hospital stay was significantly shorter in the study group than in the control group (p< 0.05). Compared with before nursing, the health knowledge, self-care skills, self-responsibility and self-concept of two groups were strongly increased after nursing, and the study group had much higher indexes than the control group (p< 0.05). After nursing, the levels of MBP, S100B, GFAP, NSE, Asp, NPY, SP and Glu in both groups were largely decreased, and more significant decrease was found in the study group (p< 0.05). Age, body mass index (BMI), hypertension history, coronary heart disease history and National Institutes of Health Stroke Score (NIHSS) score after treatment were significantly different between the good and poor prognosis groups (p< 0.05). The prognosis of patients in the study group was 52.73%, which was significantly higher than 32.73% in the control group (p< 0.05). Age, hypertension history, and post-treatment NIHSS score were independent risk factors related to poor prognosis by logistic multiple regression analysis (p< 0.05). CONCLUSIONS: Comprehensive care measures of HAPA model may be used with advantage to improve the self-care ability, reduce the degree of neurological damage, and improve neurological function in cerebral infarction patients. Age, hypertension history, and NIHSS score after treatment were all risk factors related to poor prognosis.

A case of moyamoya disease diagnosed as cerebral infarction in the early postpregnancy period and surgically treated by bilateral revascularization after term delivery.

We treated a 37-year-old Japanese woman with moyamoya disease who developed cerebral infarction in the early period after pregnancy and had undergone infertility treatment. After being adequately informed, including regarding the risk of stroke in the perinatal period and the option to prioritize the treatment of moyamoya disease even if the pregnancy was interrupted, the patient decided to continue the pregnancy and underwent surgical treatment after a full-term delivery by caesarean section. No new stroke was observed throughout the perinatal period or postoperative course. Since serious stroke during the perinatal period has also been reported in moyamoya disease, it is important to plan "tailored" treatment by sufficiently informing patients considering individual backgrounds and for multiple medical departments, including obstetrics, neurology, and neurosurgery departments, to carry out close outpatient follow-up in the perinatal period and carefully careful medication usage and radiological examinations.

Neuroinflammation-associated miR-106a-5p serves as a biomarker for the diagnosis and prognosis of acute cerebral infarction.

BACKGROUND: Acute cerebral infarction (ACI) is a common cerebrovascular disease. Previous studies have shown that some abnormally expressed microRNAs (miRNAs) play important roles in ACI. This study aimed to investigate the role of miR-106a-5p in the diagnosis and prognosis of ACI patients, and analyze the regulatory potential of miR-106a-5p on the inflammation of BV-2 microglial cells. METHOD: Serum and cerebrospinal fluid (CSF) samples were collected from 98 ACI patients, and the expression of serum miR-106a-5p was analyzed using qRT-PCR. A receiver operating characteristic (ROC) curve analysis was used to evaluate the diagnostic value of miR-106a-5p. The association of miR-106a-5p with ACI prognosis was evaluated using the logistic analysis. In vitro experiments were performed in BV-2 cells by oxygen glucose deprivation (OGD) treatment, and the effects of miR-106a-5p on BV-2 inflammation were assessed using an enzyme linked immunosorbent assay (ELISA). RESULT: It was observed that miR-106a-5p was significantly upregulated in the serum and CSF of ACI patients (all P < 0.001), and had considerable diagnostic accuracy. The highest serum miR-106a-5p was observed in severe ACI cases, and miR-106a-5p expression was significantly increased in unfavorable prognosis patients. Serum and CSF expression of miR-106a-5p was positively correlated with proinflammatory cytokines in ACI patients, and the inflammation of OGD-induced BV-2 cells was suppressed by miR-106a-5p reduction. CONCLUSION: MiR-106a-5p is overexpressed in ACI patients and may serve as a diagnostic and prognostic biomarker for ACI. Furthermore, miR-106a-5p may be involved in ACI progression by regulating neuroinflammation.

Frequency and Pattern of MRI Diffusion Restrictions after Diagnostic Catheter Neuroangiography.

(1) Background: We investigated the frequency, location, and lesion size of diffusion restrictions (DR) in magnetic resonance imaging (MRI) of asymptomatic patients after diagnostic angiography and assessed risk factors for their occurrence. (2) Methods: We analyzed diffusion-weighted images (DWI) of 344 patients undergoing diagnostic angiographies in a neuroradiologic center. Only asymptomatic patients who received a magnetic resonance imaging (MRI) examination within seven days after the angiography were included. (3) Results: Asymptomatic infarcts on DWI were identified in 17% of the cases after diagnostic angiography. In these 59 patients, a total of 167 lesions were noted. The diameter of the lesions was 1-5 mm in 128 lesions, and 5-10 mm in 39 cases. Dot-shaped diffusion restrictions were found most frequently (n = 163, 97.6%). None of the patients had neurological deficits during or after angiography. Significant correlations were found between the occurrence of lesions and patient age (p < 0.001), history of atherosclerosis (p = 0.014), cerebral infarction (p = 0.026), or coronary heart disease/heart attack (p = 0.027); and the amount of contrast medium used (p = 0.047) and fluoroscopy time (p = 0.033). (4) Conclusions: With an incidence of 17%, we observed a comparatively high risk for asymptomatic cerebral ischemia after diagnostic neuroangiography. Further measures to reduce the risk of silent embolic infarcts and improve the safety of neuroangiography are warranted.

Leukoaraiosis severity is related to increased risk of early neurological deterioration in acute ischemic stroke: a retrospective observational study.

OBJECTIVES: The relationship between leukoaraiosis and early neurological deterioration in acute cerebral infarction patients remains controversial. We tried to determine whether an association existed between leukoaraiosis and early neurological deterioration in patients with acute ischemic stroke. MATERIALS AND METHODS: We retrospectively enrolled acute cerebral infarction patients admitted to our our department within 4.5-72.0 h of symptom onset between January 2016 and March 2022. On the basis of the van Swieten scale, leukoaraiosis was evaluated as supratentorial white matter hypoattenuation on admission head CT and graded as 0 (absent), 1 (mild), 2 (moderate) and 3-4 (severe). Early neurological deterioration was defined as an increase in the National Institute of Health Stroke Scale score by > = 2 points in the total score, or > = 1 point in motor power within the first seven days after admission. RESULTS: Among 736 patients, 522 (70.9%) patients had leukoaraiosis, and of these, 332 (63.6%) had mild leukoaraiosis, 41 (7.9%) had moderate leukoaraiosis, and 149 (28.5%) had severe leukoaraiosis. 118 (16.0%) patients experienced early neurological deterioration: 20 of the 214 (9.5%) patients without leukoaraiosis and 98 of the 522 (18.8%) patients with leukoaraiosis. In multiple regression analysis, we found van Swieten scale predicted early neurological deterioration independently (OR = 1.570; 95% CI: 1.226-2.012). CONCLUSIONS: Leukoaraiosis is common in acute cerebral infarction patients and leukoaraiosis severity is related to increased risk of early neurological deterioration in the patients.

Development and usability of a hospital standardized ADL ratio (HSAR) for elderly patients with cerebral infarction: a retrospective observational study using administrative claim data from 2012 to 2019 in Japan.

BACKGROUND: Maintenance of activities of daily living (ADL) during acute hospitalization is an important treatment goal, especially for elderly inpatients with diseases that often leave disabilities, such as cerebral infarction. However, studies assessing risk-adjusted ADL changes are limited. In this study, we developed and calculated a hospital standardized ADL ratio (HSAR) using Japanese administrative claims data to measure the quality of hospitalization care for patients with cerebral infarction. METHODS: This study was designed as a retrospective observational study using the Japanese administrative claim data from 2012 to 2019. The data of all hospital admissions with a primary diagnosis of cerebral infarction (ICD-10, I63) were used. The HSAR was defined as the ratio of the observed number of ADL maintenance patients to the expected number of ADL maintenance patients multiplied by 100, and ratio of ADL maintenance patients was risk-adjusted using multivariable logistic regression analyses. The c-statistic was used to evaluate the predictive accuracy of the logistic models. Changes in HSARs in each consecutive period were assessed using Spearman's correlation coefficient. RESULTS: A total of 36,401 patients from 22 hospitals were included in this study. All variables used in the analyses were associated with ADL maintenance, and evaluations using the HSAR model showed predictive ability with c-statistics (area under the curve, 0.89; 95% confidence interval, 0.88-0.89). CONCLUSIONS: The findings indicated a need to support hospitals with a low HSAR because hospitals with high/low HSAR were likely to produce the same results in the subsequent periods. HSAR can be used as a new quality indicator of in-hospital care and may contribute to the assessment and improvement of the quality of care.

Case report: Autoimmune encephalitis associated with anti-CASPR2 antibody mimicking cerebral infarction.

Autoimmune encephalitis associated with antibody against contactin-associated protein-like 2 (CASPR2) varies in its clinical presentation. The disease is difficult to distinguish from some other conditions without testing for anti-CASPR2 antibody in blood serum or cerebrospinal fluid. Cerebral lesions are typically detected by magnetic resonance imaging (MRI) in the medial temporal lobe or hippocampus. Here, we describe a patient with anti-CASPR2 antibody autoimmune encephalitis whose imaging manifestations mimicked infarction in the left frontal lobe. The 48-year-old man reported memory loss, convulsions, and disturbed consciousness one day after drinking wine. The right upper arm showed reduced autonomous movement after painful stimuli, and MRI showed abnormal hyperintensities in the left frontal lobe on T2 and fluid-attenuated inversion recovery sequences, restricted diffusion, and decreased cerebral blood flow, mimicking acute cerebral infarction. Contrast-enhanced T1-weighted MRI showed gyral enhancement involving the cortex and subcortical white matter. Computed tomography angiography did not identify culprit blood vessels. Symptoms did not improve with anti-platelet or lipid-lowering therapy. Screening for serum antibodies associated with autoimmune encephalitis detected antibody against CASPR2, and intravenous immunoglobulin therapy substantially improved symptoms. This case provides the first indication that anti-CASPR2 antibody-associated autoimmune encephalitis can manifest as involvement of the cortex and subcortical white matter in the frontal lobe based on MRI. It emphasizes the need for thorough investigation, including analysis of potential autoimmunity, of patients whose imaging findings mimic ischemic infarction.

Diagnostic value and mechanism of plasma S100A1 protein in acute ischemic stroke: a prospective and observational study.

Background: Plasma S100A1 protein is a novel inflammatory biomarker associated with acute myocardial infarction and neurodegenerative disease's pathophysiological mechanisms. This study aimed to determine the levels of this protein in patients with acute ischemic stroke early in the disease progression and to investigate its role in the pathogenesis of acute ischemic stroke. Methods: A total of 192 participants from hospital stroke centers were collected for the study. Clinically pertinent data were recorded. The volume of the cerebral infarction was calculated according to the Pullicino formula. Multivariate logistic regression analysis was used to select independent influences. ROC curve was used to analyze the diagnostic value of AIS and TIA. The correlation between S100A1, NF-κB p65, and IL-6 levels and cerebral infarction volume was detected by Pearson correlation analysis. Results: There were statistically significant differences in S100A1, NF-κB p65, and IL-6 among the AIS,TIA, and PE groups (S100A1, [230.96 ± 39.37] vs [185.85 ± 43.24] vs [181.47 ± 27.39], P < 0.001; NF-κB p65, [3.99 ± 0.65] vs [3.58 ± 0.74] vs [3.51 ± 0.99], P = 0.001; IL-6, [13.32 ± 1.57] vs [11.61 ± 1.67] vs [11.42 ± 2.34], P < 0.001). Multivariate logistic regression analysis showed that S100A1 might be an independent predictive factor for the diagnosis of disease (P < 0.001). The AUC of S100A1 for diagnosis of AIS was 0.818 (P < 0.001, 95% CI [0.749-0.887], cut off 181.03, Jmax 0.578, Se 95.0%, Sp 62.7%). The AUC of S100A1 for diagnosis of TIA was 0.720 (P = 0.001, 95% CI [0.592-0.848], cut off 150.14, Jmax 0.442, Se 50.0%, Sp 94.2%). There were statistically significant differences in S100A1, NF-κB p65, and IL-6 among the SCI,MCI, and LCI groups (S100A1, [223.98 ± 40.21] vs [225.42 ± 30.92] vs [254.25 ± 37.07], P = 0.001; NF-κB p65, [3.88 ± 0.66] vs [3.85 ± 0.64] vs [4.41 ± 0.45], P < 0.001; IL-6, [13.27 ± 1.65] vs [12.77 ± 1.31] vs [14.00 ± 1.40], P = 0.007). Plasma S100A1, NF-κB p65, and IL-6 were significantly different from cerebral infarction volume (S100A1, r = 0.259, P = 0.002; NF-κB p65, r = 0.316, P < 0.001; IL-6, r = 0.177, P = 0.036). There was a positive correlation between plasma S100A1 and IL-6 with statistical significance (R = 0.353, P < 0.001). There was no significant positive correlation between plasma S100A1 and NF-κB p65 (R < 0.3), but there was statistical significance (R = 0.290, P < 0.001). There was a positive correlation between IL-6 and NF-κB p65 with statistical significance (R = 0.313, P < 0.001). Conclusion: S100A1 might have a better diagnostic efficacy for AIS and TIA. S100A1 was associated with infarct volume in AIS, and its level reflected the severity of acute cerebral infarction to a certain extent. There was a correlation between S100A1 and IL-6 and NF-κB p65, and it was reasonable to speculate that this protein might mediate the inflammatory response through the NF-κB pathway during the pathophysiology of AIS.

Epiglottic Cyst With Slurred Speech Misdiagnosed as Acute Cerebral Infarction: A Case Report.

INTRODUCTION: Epiglottic cysts are cysts that occur under the mucosa of the epiglottis. Patients with severe cysts may have difficulty in breathing. Slurred speech usually occurs in cerebrovascular diseases, especially with slurred speech as the starting symptom. CASE REPORT: We describe the case of a patient with slurred speech as the first symptom. The patient was a 53-year-old man with slurred speech as the first symptom, and he was initially considered to have an acute cerebral infarction. However, the results of the cranial magnetic resonance imaging examination did not support the diagnosis. The possibility of neck tumor recurrence was considered based on past medical history. The findings of a computed tomography examination of the neck suggested an epiglottic cyst. The effect of anti-inflammatory and surgical treatment was significant, and speech returned to normal. CONCLUSION: This case emphasizes that neurologists need to be vigilant when dealing with patients with slurred speech, which may be one of the clinical manifestations of epiglottic cysts.

Comparison of frequency of silent cerebral infarction as assessed by serum neuron specific enolase in patients with non-valvular atrial fibrillation: Warfarin versus direct oral anticoagulant.

BACKGROUND: Cerebral infarction in patients with atrial fibrillation (AF) may clinically vary from being silent to catastrophic. Silent cerebral infarction (SCI) is the neuronal injury in the absence of clinically appearent stroke or transient ischaemic attack. Serum neuron specific enolase (NSE) is suggested to be a valid surrogate biomarker that allows to detect recent neuronal injury. We aimed to evaluate the incidence of recent SCI by positive NSE levels in patients with non-valvular AF (NVAF) on oral anticoagulants. METHODS: Blood samples for NSE were collected from 197 consecutive NVAF patients. NSE levels of greater than 12 ng/ml was considered as positive and suggestive of SCI. RESULTS: Patients were mainly female with a mean age of 69 years. Ninety-eight of them (49.7%) were taking warfarin. Mean INR level was 2.3 ± 0.9. Mean CHA2DS2-VASc score of the study population was 3.5 ± 1.5. Seventy-two patients (36.5%) were found to have NSE elevation. They were more likely to have history of chronic heart failure and previous stroke/TIA. Increased left atrial diameter and higher CHA2DS2-VASc were other factors associated with SCI. Patients on DOACs and patients taking aspirin on top of oral anticoagulant treatment were less likely to have SCI. Multivariate analysis demonstrated that increased left atrial diameter (OR: 2.5; 95% CI: 1.52-4; p < 0.001) and use of warfarin (OR: 2.8; 95% CI: 1.37-5.61; p = 0.005) were detected as independent predictors of SCI. CONCLUSIONS: Our study revealed that DOACs were associated with significantly reduced SCIs compared with warfarin, probably due to more effective and consistent therapeutic level of anticoagulation.