Impact of serum leptin and adiponectin levels on brain infarcts in patients with mild cognitive impairment and Alzheimer's disease: a longitudinal analysis.

Introduction: The adipokines leptin and adiponectin have been associated with atherosclerosis and the risk of cerebral infarcts. Pre-clinical studies, however, suggest a protective role against ischemic brain damage. In this study we analyzed the relationship between serum leptin and adiponectin levels and the onset or progression of brain infarcts in subjects with mild cognitive impairment (MCI) and Alzheimer's disease (AD). Methods: All data were extracted from the ADNI database. The final population included 566 subjects, with 58 healthy controls, 396 MCI and 112 AD. All patients with available serum leptin and adiponectin levels at baseline were selected. Demographics, neuropsychological test results, CSF biomarkers, regional brain metabolism with FDG-PET data and the number of brain infarcts on longitudinal MRI scans were extracted. Results: Leptin levels were significantly lower in patients with MCI than controls at baseline, while adiponectin levels were not different between the groups. Multivariate logistic regression analysis at baseline for the presence of brain infarcts showed a predictive value for leptin but not for adiponectin. Multivariate longitudinal analysis showed that age was the only significant predictor of brain infarcts development at 15-year follow-up, while serum leptin and adiponectin levels did not play a role in this population. Discussion: The evidence on the pathogenetic or protective role of adipokines on ischemic brain damage is mixed. In this MCI and AD population, serum leptin and adiponectin were not associated with the development of brain infarcts; therefore, these results do not support the use of adipokines as biomarkers of cerebrovascular pathology in this population.

Plasma Neurofilament Light Chain Is Elevated after Transcatheter Aortic Valve Implantation.

INTRODUCTION: Transcatheter aortic valve implantation (TAVI) is associated with a high incidence of new silent brain infarcts (SBIs) on postprocedural neuroimaging. A venous blood sample reflecting neuronal damage following TAVI could help identify patients with potential SBIs. We aimed to investigate if a biochemical marker of neuronal injury, neurofilament light chain (NFL), is elevated after TAVI. METHODS: In this observational study, NFL was measured in plasma from 31 patients before and after TAVI. Multivariable regression analysis was performed to investigate any effect of clinical- and procedure-related factors on differences in NFL levels before and after TAVI. RESULTS: Samples were collected 41 (14-81) days before and 44 (35-59) days after TAVI, median (interquartile range). Median age was 81 (77-84) years, and 35% were female. No patient had any overt procedure-related neurological complications. The geometric mean (95% confidence interval) of the NFL concentration was 30 (25-36) pg/mL before TAVI and 48 (39-61) pg/mL, after TAVI, p <0.001. None of the included variables in the multiple linear regression model were statistically significantly associated with the difference in levels before and after TAVI. CONCLUSIONS: NFL levels in plasma were higher after TAVI as compared with levels before, with a mean increase of 60% (18 pg/mL). Further studies including neuroimaging and cognitive outcomes are needed to understand the potential value of measuring NFL in relation to TAVI.

The Diagnostic Value of Whole Blood lncRNA NR_120420 for Acute Ischemic Stroke.

OBJECTIVE: Current clinical practice based on CT or multimodal images to diagnose ischemic stroke always led to substantial treatment delay. We perform this study to explore possible circulating lncRNA biomarker to help promptly diagnose the disease. METHODS: We used microarray to identify the differentially expressed lncRNAs in the peripheral whole blood between AIS patients and controls and verified the results by quantitative polymerase chain reaction (qPCR). Multivariate logistic regressions were performed to determinate the lncRNAs independently associated with AIS occurrence. The ROC curve was used to detect the diagnostic accuracy of candidate lncRNAs in AIS and AIS subtypes, which was classified according to the Oxford Community Stroke Project (OCSP) criteria. RESULTS: The microarray analysis screened out 5686 differentially expressed lncRNAs. Among the nine selected lncRNAs verified by qPCR, NR_120420 (OR 1.29, 95% CI 1.02-1.65, P = 0.037) was found independently associated with AIS after balancing patient baseline characteristics. The receiver operating characteristic (ROC) analysis concerning NR_120420 in total anterior circulation infarction subgroup showed that the area under the curve was 0.86 (95% CI: 0.73-0.99, P = 0.003), and at the optimal cutoff point of 1.93, the sensitivity and specificity reached 85.7% and 84.6%, respectively. CONCLUSION: Our study indicated that NR_120420 could predict the total anterior circulation infarction with high sensitivity and specificity and could be potentially used as a biomarker for total anterior circulation infarction in AIS patients.

Urea-Creatinine Ratio (UCR) After Aneurysmal Subarachnoid Hemorrhage: Association of Protein Catabolism with Complication Rate and Outcome.

OBJECTIVE: The urea-creatinine ratio (UCR) has been proposed as potential biomarker for critical illness-associated catabolism. Its role in the context of aneurysmal subarachnoid hemorrhage (aSAH) remains to be elucidated, which was the aim of the present study. METHODS: We enrolled 66 patients with aSAH with normal renal function and 36 patients undergoing elective cardiac surgery as a control group for the effects of surgery. In patients with aSAH, the predictive or diagnostic value of early (day 0-2) and critical (day 5-7) UCRs was assessed with regard to delayed cerebral ischemia (DCI), DCI-related infarction, and clinical outcome after 12 months. RESULTS: Preoperatively, UCR was similar both groups. Within 2 days postoperatively, UCRs increased significantly in patients in the elective cardiac surgery group (P < 0.001) but decreased back to baseline on day 5-7 (P = 0.245), whereas UCRs in patients with aSAH increased to significantly greater levels on day 5-7 (P = 0.028). Greater early or critical UCRs were associated with poor clinical outcomes (P = 0.015) or DCI (P = 0.011), DCI-related infarction (P = 0.006), and poor clinical outcomes (P < 0.001) respectively. In multivariate analysis, there was an independent association between greater early UCRs and poor clinical outcomes (P = 0.026). CONCLUSIONS: In this exploratory study of UCR in the context of aSAH, greater early values were predictive for a poor clinical outcome after 12 months, whereas greater critical values were associated with DCI, DCI-related infarctions, and poor clinical outcomes. The clinical implications as well as the pathophysiologic relevance of protein catabolism should be explored further in the context of aSAH.

Endocan: A Novel Predictor of Endothelial Dysfunction in Silent Brain Infarction.

Silent brain infarction (SBI) has been considered as a subclinical risk factor for symptomatic possible future stroke. We investigated the association between serum inflammatory markers and SBI. Patients (n = 54) diagnosed with SBI as the study group and 52 individuals as the control group were included in this study. Silent brain infarction is defined as a hyperintense lesion that was ≥3 mm in 1 dimension on fluid-attenuated inversion recovery T2-weighted magnetic resonance image, if the patient had normal neurological examination or had an abnormality that was not consistent with the brain lesion locations, after being evaluated by a neurologist. Serum endocan levels (P = .036) and high-sensitivity C-reactive protein (hsCRP; P = .022) were significantly higher in patients with SBI than the controls. Pentraxin 3, erythrocyte sedimentation rate, white blood count, lymphocyte, monocyte, neutrophil, low-density lipoprotein, and triglyceride levels were not significantly different when comparing the groups with and without SBI. There was a significant correlation (r = -0.196; P = .16) between hsCRP and endocan levels in the SBI group. Endocan, a novel biomarker of endothelial pathology, was significantly increased in patients with SBI and may be useful to predict the future risk of stroke.

Metformin prevents stroke damage in non-diabetic female mice with chronic kidney disease.

Chronic kidney disease (CKD) worsens ischemic stroke severity in both patients and animals. In mice, these poorer functional outcomes are associated with decreased brain activity of AMP-activated protein kinase (AMPK), a molecule that recently emerged as a potential therapeutic target for ischemic stroke. The antidiabetic drug metformin, a well-known activator of AMPK, has improved stroke outcomes in diabetic patients with normal renal function. We investigated whether chronic metformin pre-conditioning can rescue AMPK activity and prevent stroke damage in non-diabetic mice with CKD. Eight-week-old female C57BL/6J mice were assigned to CKD or SHAM groups. CKD was induced through right kidney cortical electrocautery, followed by left total nephrectomy. Mice were then allocated to receive metformin (200 mg/kg/day) or vehicle for 5 weeks until stroke induction by transient middle cerebral artery occlusion (tMCAO). The infarct volumes were lower in CKD mice exposed to metformin than in vehicle-treated CKD mice 24 h after tMCAO. Metformin pre-conditioning of CKD mice improved their neurological score, grip strength, and prehensile abilities. It also enhanced AMPK activation, reduced apoptosis, increased neuron survival and decreased microglia/macrophage M1 signature gene expression as well as CKD-induced activation of the canonical NF-κB pathway in the ischemic lesions of CKD mice.

The Omega-3 Fatty Acid Eicosapentaenoic Acid (EPA) Correlates Inversely with Ischemic Brain Infarcts in Patients with Atrial Fibrillation.

The omega-3 fatty acid (n-3 FA) eicosapentaenoic acid (EPA) reduces stroke in patients with atherosclerotic cardiovascular disease. Whether EPA affects stroke or cerebral small vessel dis-ease in patients with atrial fibrillation (AF) remains uncertain. EPA, docosahexaenoic acid (DHA), docosapentaenoic acid (DPA), and alpha-linolenic acid (ALA) were determined by gas chromatography in 1657 AF patients from the Swiss Atrial Fibrillation study. All patients underwent brain MRI to detect ischemic brain infarcts, classified as large noncortical or cortical infarcts (LNCCIs); markers of small vessel disease, classified as small noncortical infarcts (SNCIs), number of microbleeds, and white matter lesion (WML) volumes. Individual and total n-3 FAs (EPA + DHA + DPA + ALA) were correlated with LNCCIs and SNCIs using logistic regression, with numbers of microbleeds using a hurdle model, and WML volumes using linear regression. LNCCIs were detected in 372 patients (22.5%). EPA correlated inversely with the prevalence of LNCCIs (odds ratio [OR] 0.51 per increase of 1 percentage point EPA, 95% confidence interval [CI] 0.29-0.90). DPA correlated with a higher LNCCI prevalence (OR 2.48, 95%CI 1.49-4.13). No associations with LNCCIs were found for DHA, ALA, and total n-3 FAs. Neither individual nor total n-3 FAs correlated with markers of small vessel disease. In conclusion, EPA correlates inversely with the prevalence of ischemic brain infarcts, but not with markers of small vessel disease in patients with AF.

Recovery of Hypoxic Regions in a Rat Model of Microembolism.

OBJECTIVES: Endovascular treatment (EVT) has become the standard of care for acute ischemic stroke. Despite successful recanalization, a limited subset of patients benefits from the new treatment. Human MRI studies have shown that during removal of the thrombus, a shower of microclots is released from the initial thrombus, possibly causing new ischemic lesions. The aim of the current study is to quantify tissue damage following microembolism. MATERIALS AND METHODS: In a rat model, microembolism was generated by injection of a mixture of polystyrene fluorescent microspheres (15, 25 and 50 µm in diameter). The animals were killed at three time-points: day 1, 3 or 7. AMIRA and IMARIS software was used for 3D reconstruction of brain structure and damage, respectively. CONCLUSIONS: Microembolism induces ischemia, hypoxia and infarction. Infarcted areas persist, but hypoxic regions recover over time suggesting that repair processes in the brain rescue the regions at risk.

CT assessment of the increased density of cerebral vessels in plateau region.

In this study, the relationship between the brain parenchymal density, the cerebral vessel density, the mean corpuscular hemoglobin (MCH) content, the mean corpuscular hemoglobin concentration (MCHC), and the morbidity associated with lacunar infarction of residents living in either the plains or the plateau regions were analyzed and compared for their potential clinical implications. Clinical data from the brain CT scans of individuals living in either the plain or plateau regions (129 each) were collected. Specifically, the CT values for basal ganglia, the middle cerebral artery, and the superior sagittal sinus, along with the number of patients with lacunar infarction, were collected. In addition, the MCH and MCHC values were measured in blood samples collected within 48 h following the CT scans. For statistical analysis, an independent sample t-test, Pearson's correlation test (permutation test), and Chi-squared test were employed. The inhabitants of the plateau had a significantly higher CT value of basal ganglia, the middle cerebral artery, and superior sagittal sinus and also higher levels of MCH and MCHC in the blood (ps < 0.001) than the inhabitants of the plains region. Further, there was a significant positive correlation between the three aforementioned CT values and the MCH and MCHC findings. However, no significant differences were found in the morbidity of lacunar infarction between these two regions (p > 0.05). The inhabitants in the plateau have a significantly higher brain parenchymal density, higher CT value for cerebral vessels density, and higher blood MCH and MCHC levels in comparison with individuals occupying the plains. Concurrently, the parenchymal density and the CT values are shown to be positively correlated with the MCH and MCHC content in the blood.

Risk factors for acute stroke-associated pneumonia and prediction of neutrophil-to-lymphocyte ratios.

OBJECTIVES: This study aimed to analyze the risk factors for stroke-associated pneumonia (SAP) and assess the predictive effect of neutrophil-to-lymphocyte ratio (NLR) on acute SAP. METHODS: The study included acute stroke patients from April 2018 to June 2019. These patients were divided into the SAP and Non-SAP groups. The patients' history of chronic diseases was assessed, including history of hypertension, diabetes, hyperlipidemia, chronic lung disease, and current smoking status. The clinical characteristics of all studied cases were recorded, including the initial stroke type (cerebral infarction or cerebral hemorrhage), National Institute of Health Stroke Scale (NIHSS) score, indwelling nasogastric tubes, stroke-associated pneumonia within 7 days of hospitalization, and length of hospitalization. The study also recorded the laboratory testing data, including fasting blood glucose, triglyceride, total cholesterol, low-density lipoprotein cholesterol, glycosylated hemoglobin, and high-sensitivity C-reactive protein (hsCRP) as well as white blood cell (WBC), neutrophil, and lymphocyte counts. SPSS 19.0 was used for statistical analysis. RESULTS: A total of 328 eligible acute stroke patients were included. Among all participants, SAP occurred in 64 (19.5%) patients. In the SAP group, the patients were older, the proportion of cerebral hemorrhage was higher, the NIHSS score was higher, and more patients had nasogastric tubes (P < 0.05). Concomitantly, the blood glucose, hsCRP, WBC count, neutrophil count, and NLR of the SAP group were significantly higher than those of the Non-SAP group, whereas the lymphocyte count was significantly lower than that of the Non-SAP group (P < 0.05). Multivariable analysis of Binary Logistic regression revealed that stroke type (cerebral hemorrhage), indwelling gastric tube, and NLR were independent risk factors for SAP. Receiver operating characteristic curve analysis demonstrated that the area under the curve for the NLR's ability to predict SAP was 0.861. The optimal cutoff threshold, sensitivity, and specificity were 3.745, 0.891, and 0.727, respectively. CONCLUSIONS: The risk factors for SAP were multifaceted. Cerebral hemorrhage, indwelling nasogastric tube, and high NLR were independent risk factors. An early NLR had a predictive effect on the occurrence of SAP in patients with acute stroke.

Higher level of acute serum VEGF and larger infarct volume are more frequently associated with post-stroke cognitive impairment.

BACKGROUND: Serum vascular endothelial growth factor (VEGF) and infarct volume detected by brain imaging have been associated with stroke outcome. However, the relationship of these two variables with post-stroke cognitive impairment (PSCI) remains unclear. We aimed to investigate the association between acute serum VEGF levels and infarct volume with PSCI in ischemic stroke patients. METHODS: Fifty-six first-ever ischemic stroke patients who were hospitalized in Dr. Sardjito General Hospital Yogyakarta, Indonesia were prospectively recruited. Serum VEGF level was taken on day 5 of stroke onset and measured by ELISA. Infarct volume was calculated manually from head CT scan by expert radiologist. PSCI was assessed after 3 months follow up by using Montreal Cognitive Assessment-Indonesian version (MoCA-INA). We performed a ROC curve analysis to determine the cut-off point of VEGF level and infarct volume. Multivariate logistic regression analysis was performed to measure the contribution of VEGF level and infarct volume to PSCI after controlling covariates (demographic and clinical data). RESULTS: The mean age of PSCI and non-PSCI patients was 61.63% ± 8.47 years and 58.67% ± 9.01 years, respectively (p = 0.221). No differences observed for vascular risk factors, infarct location, and NIHSS in both groups. Multivariate logistic regression showed that patients with higher VEGF level alone (≥519.8 pg/ml) were 4.99 times more likely to have PSCI than those with lower VEGF level (OR = 4.99, 95% CI = 1.01-24.7, p = 0.048). In addition, patients with larger infarct volume alone (≥0.054 ml) were also more frequently associated with PSCI (OR = 7.71, 95% CI = 1.39-42.91, p = 0.019). CONCLUSIONS: Acute ischemic stroke patients with higher serum VEGF level (≥519.8 pg/ml) and larger infarct volume (≥0.054 ml) were more likely to have PSCI 3 months after stroke. These findings may contribute to predict PSCI earlier and thus better prevention strategy could be made.

Association of Serum Complement C1q Concentration with Severity of Neurological Impairment and Infarct size in Patients with Acute Ischemic Stroke.

BACKGROUND: Inflammation occurs after acute ischemic stroke (AIS), and complement C1q is involved in inflammation. However, studies about the association of complement C1q with AIS are still rare. The aim of our study is to investigate the relationship between serum C1q concentration and the clinical severity of AIS. METHODS: A total of 1294 patients were enrolled in our study, including 647 patients with AIS and 647 non-stroke controls. The infarction volume of AIS was assessed by the diameter of maximum transverse section (DMTS) based on diffusion-weighted imaging (DWI) of brain magnetic resonance imaging. Neurological impairment was assessed by the National Institute of Health Stroke Scale (NIHSS). The association of serum C1q levels with DMTS or NIHSS was investigated by Pearson's or Spearman's correlation analysis. RESULTS: Serum C1q levels of patients with AIS were significantly higher than those of individuals without AIS. Serum levels of C1q were associated with DMTS (r=0.511, p<0.001) and NIHSS (r=0.433, p<0.001) among patients with AIS. CONCLUSION: Serum C1q concentration was positively associated with DMTS and NIHSS of patients with AIS.

Early neutrophil count relates to infarct size and fatal outcome after large hemispheric infarction.

AIMS: To investigate the relationship between peripheral leukocyte dynamics and the outcome of large hemispheric infarction (LHI) patients. METHODS: Patients with acute LHI admitted to the neuro-intensive care unit of Xuanwu Hospital from 2013 to 2017 were prospectively enrolled and followed up for 6 months after LHI. RESULTS: A total of 84 LHI patients were included, 38 patients suffered brain herniation and 20 patients died from stroke. Compared to patients with benign course, LHI patients with fatal outcome showed larger infarcts and more severe brain edema (P < .01), as well as increased WBC and neutrophil counts throughout the first week after stroke (P < .05). Correlation analysis revealed that neutrophil counts on D2 after LHI positively correlated with infarct and edema volumes measured from CT/MRI (R2  = 0.22 and R2  = 0.15, P < .01) and negatively correlated with Glasgow Coma Scale (ρ = -0.234, P < .05). Patients with D2 neutrophils > 7.14 × 109 /L had higher risk of brain herniation [odds ratio (OR) = 7.5, 95% CI: 2.0-28.1, P = .001], and patients with D2 neutrophils > 7.79 × 109 /L had a higher risk of death (OR = 5.8, 95% CI: 1.2-27.0, P = .015). CONCLUSION: Early peripheral neutrophil count after stroke relates to infarct size and the fatal outcome of LHI patients, which might help guiding acute LHI management such as reduction of intracranial pressure and potential antiinflammatory therapy in the future.

Atrial Cardiopathy and Nonstenosing Large Artery Plaque in Patients With Embolic Stroke of Undetermined Source.

Background and Purpose- Atrial cardiopathy and atherosclerotic plaque are two potential mechanisms underlying embolic strokes of undetermined source (ESUS). The relationship between these two mechanisms among ESUS patients remains unclear. A better understanding of their association may inform targeted secondary prevention strategies. Methods- We examined the association between atrial cardiopathy and atherosclerotic plaque in the NAVIGATE ESUS trial (New Approach Rivaroxaban Inhibition of Factor Xa in a Global Trial Versus ASA to Prevent Embolism in Embolic Stroke of Undetermined Source), which enrolled 7213 patients with recent ESUS during 2014 to 2017. For this analysis, we included patients with data on left atrial dimension, location of brain infarction, and cervical large artery plaque. The variables of primary interest were left atrial diameter and cervical plaque ipsilateral to brain infarction. Secondary markers of atrial cardiopathy were premature atrial contractions on Holter monitoring and newly diagnosed atrial fibrillation. For descriptive purposes, left atrial enlargement was defined as ≥4.7 cm. Multivariable logistic regression was used to examine the association between atrial cardiopathy markers and ipsilateral plaque after adjustment for age, sex, body mass index, hypertension, diabetes mellitus, current smoking, and hyperlipidemia. Results- Among 3983 eligible patients, 235 (5.9%) had left atrial enlargement, 939 (23.6%) had ipsilateral plaque, and 94 (2.4%) had both. Shared risk factors for left atrial enlargement and ipsilateral plaque were male sex, white race, hypertension, tobacco use, and coronary artery disease. Despite shared risk factors, increasing left atrial dimension was not associated with ipsilateral plaque after adjustment for covariates (odds ratio per cm, 1.1 [95% CI, 1.0-1.2]; P=0.08). We found no consistent associations between secondary markers of atrial cardiopathy and ipsilateral plaque. Conclusions- In a large population of patients with ESUS, we did not observe a notable association between atrial cardiopathy and atherosclerotic plaque, and few patients had both conditions. These findings suggest that atrial cardiopathy and atherosclerotic plaque may be distinct, nonoverlapping risk factors for stroke among ESUS patients.

Assessing acrolein for determination of the severity of brain stroke, dementia, renal failure, and Sjögren's syndrome.

It was found recently that acrolein (CH2=CH-CHO), mainly produced from spermine, is more toxic than ROS (reactive oxygen species, O2-·, H2O2, and ·OH). In this review, we describe how the seriousness of brain infarction, dementia, renal failure, and SjÓ§gren's syndrome is correlated with acrolein. In brain infarction and dementia, it was possible to identify incipient patients with high sensitivity and specificity by measuring protein-conjugated acrolein (PC-Acro) in plasma together with IL-6 and CRP in brain infarction and Aß40/42 in dementia. The level of PC-Acro in plasma and saliva correlated with the seriousness of renal failure and SjÓ§gren's syndrome, respectively. Thus, development of acrolein scavenger medicines containing SH-group such as N-acetylcysteine derivatives is important to maintain QOL (quality of life) of the elderly.

Cholesterol Variability and Cranial Magnetic Resonance Imaging Findings in Older Adults: The Cardiovascular Health Study.

Background and Purpose- Serum cholesterol variability, independent of mean, has been associated with stroke, white matter hyperintensities on cranial magnetic resonance imaging (MRI), and other cardiovascular events. We sought to assess the relationship between total serum cholesterol (TC) variability and cranial MRI findings of subclinical or covert vascular brain injury in a longitudinal, population-based cohort study of older adults. Methods- In the Cardiovascular Health Study, we assessed associations between intraindividual TC mean, trend, and variability over ≈5 years with covert brain infarction (CBI) and white matter grade (WMG) on cranial MRI. Mean TC was calculated for each study participant from 4 annual TC measurements between 2 MRI scans. TC trend was calculated as the slope of the linear regression of the TC measurements, and TC variability was calculated as the SD of the residuals from the linear regression. We evaluated the association of intraindividual TC variability with incident CBI and worsening WMG between 2 MRI scans in primary analyses and with prevalent CBI number and WMG on the follow-up MRI scan in secondary analyses. Results- Among participants who were eligible for the study and free of clinical stroke before the follow-up MRI, 17.9% of 1098 had incident CBI, and 27.8% of 1351 had worsening WMG on the follow-up MRI. Mean, trend, and variability of TC were not associated with these outcomes. TC variability, independent of mean and trend, was significantly associated with the number of CBI (ß=0.009 [95% CI, 0.003-0.016] P=0.004; N=1604) and was associated with WMG (ß, 0.009 [95% CI, -0.0002 to 0.019] P=0.055; N=1602) on the follow-up MRI. Conclusions- Among older adults, TC variability was not associated with incident CBI or worsening WMG but was associated with the number of prevalent CBI on cranial MRI. More work is needed to validate and to clarify the mechanisms underlying such associations.

Postoperative hyperglycemia predicts symptomatic intracranial hemorrhage after endovascular treatment in patients with acute anterior circulation large artery occlusion.

INTRODUCTION: Acute phase hyperglycemia is independently associated with an increased risk of death and symptomatic intracranial hemorrhage (sICH) in stroke patients treated with intravenous thrombolysis. Whether postoperative hyperglycemia is an independent predictor of sICH after endovascular therapy remains unknown. Here, we assessed whether hyperglycemia after endovascular therapy can predict sICH. METHODS: Consecutive acute ischemic stroke patients who were treated with mechanical thrombectomy with or without subsequent stent implantation were analyzed. The primary outcome was the occurrence of sICH within the first 7 days after endovascular treatment. The second outcome was other forms of hemorrhagic transformation (HT), including parenchymal hematoma (PH) and parenchymal hematoma type 2 (PH-2). RESULTS: One hundred and fifty-six patients were included. Fifteen patients (9.62%) developed sICH after endovascular therapy. After adjusting for potential confounding factors, postoperative glucose values were independently associated with sICH after endovascular therapy. Furthermore, adding postoperative glucose values to conventional risk factors led to a substantial reclassification for sICH following endovascular therapy (net reclassification improvement = 28.1%; p = .014). Moreover, postoperative glucose values were found to be risk factors for PH-2. CONCLUSIONS: We found that postoperative glucose values might be an independent risk factor for sICH in patients with anterior circulation large vessel occlusion who are treated with mechanical thrombectomy. Adding postoperative glucose values to conventional risk factors could improve risk stratification for sICH following endovascular therapy.

Sudden onset of sleep caused by hypothalamic infarction: a case report.

BACKGROUND: Hypothalamic lesions, such as tumors and demyelinating diseases, reportedly cause abnormal sleepiness. However, stroke involving the hypothalamus has rarely been described. Here, we report a patient with infarction restricted to the hypothalamus who presented with sudden onset of sleep. CASE PRESENTATION: A 42-year-old woman with a history of migraine without aura presented with irresistible sleepiness and developed several episodes of sudden onset of sleep. Neurological examinations were unremarkable except for partial left Horner syndrome. Brain magnetic resonance imaging (MRI) revealed a high-intensity lesion restricted to the left hypothalamus on diffusion-weighted and fluid-attenuated inversion recovery MRI images. Cerebrospinal fluid (CSF) orexin-A levels obtained on hospital day 3 after her sleepiness had resolved were normal (337 pg/mL; normal > 200 pg/mL). Serum anti-nuclear and anti-aquaporin 4 (AQP4) antibodies and CSF myelin basic protein and oligoclonal band were negative. A small hypothalamic infarction was suspected, and the patient was treated with intravenous edaravone and argatroban, as well as oral clopidogrel. Three months later, there had been no clinical relapse, and the hypothalamic lesion had almost disappeared on follow-up MRI. No new lesion suggestive of demyelinating disease or tumor was observed. CONCLUSION: Hypothalamic stroke should be considered a cause of sudden onset of sleep.

High triglyceride/HDL cholesterol ratio is associated with silent brain infarcts in a healthy population.

BACKGROUND: Triglycerides (TG)/high-density lipoprotein (HDL) cholesterol ratio is a marker of small/dense low-density lipoprotein particles, which are closely associated with various metabolic and vascular diseases. However, the role of TG/HDL cholesterol ratio in cerebrovascular diseases has not been well studied. In this study, we evaluated the relationship between TG/HDL cholesterol ratio and the presence of silent brain infarct (SBI) in a neurologically healthy population. METHODS: We retrospectively evaluated consecutive participants in health check-ups between January 2006 and December 2013. SBI was defined as an asymptomatic, well-defined lesion with a diameter of ≥3 mm on T1- or T2-weighted images. TG/HDL cholesterol ratio was calculated after dividing absolute TG levels by absolute HDL cholesterol levels. RESULTS: Of 3172 healthy participants, 263 (8.3%) had SBI lesions. In multivariate analysis, TG/HDL cholesterol ratio was independently associated with SBI (adjusted odds ratio [aOR] = 1.16, 95% confidence interval [CI] = 1.00 to 1.34, P = 0.047). This association was prominent in males (aOR = 1.23, 95% CI = 1.03 to 1.48, P = 0.021), but not in females. In the analyses of the relationships between lipid parameters and SBI lesion burden, TG/HDL cholesterol ratio was positively correlated, and total cholesterol/TG ratio was negatively correlated with SBI lesion burden, in dose-response manners (P for trend = 0.015 and 0.002, respectively). CONCLUSIONS: The TG/HDL cholesterol ratio was positively associated with the prevalence of SBI in a neurologically healthy population.

Serum Neurofilament Light Chain Concentration Correlates with Infarct Volume but Not Prognosis in Acute Ischemic Stroke.

BACKGROUND AND PURPOSE: We studied serum neurofilaments diagnostic value in patients with acute ischemic stroke (AIS) or TIA and evaluated any correlation with symptom severity, cerebral infarction volume, aetiology, and clinical outcome. METHODS: One hundred and thirty-six patients (101 with AIS, and 35 with TIA) were included. Acute-phase serum neurofilament light chain (sNfL) was analyzed with a novel ultrasensitive single molecule array (Simoa). Cerebral infarction volume was measured from brain computed tomography in the subacute phase (>2 days). Stroke aetiology was defined by trial of ORG 10172 in acute stroke treatment classification, severity by National Institute of Health stroke scale (NIHSS) and the degree of disability by the Modified Rankin Scale (mRS) after 90 days. RESULTS: sNfL was markedly higher in patients with AIS (89.5 pg/mL [IQR: 44.7-195.3]) than with TIA (25.2 pg/mL [IQR: 14.6-48.0]), P= <.001), also after adjusting for age, NIHSS, and stroke volume (P= .003). In receiver operating characteristic analysis, sNfL concentration greater than or equal to 49 pg/mL proved to be the best cut-off value to differentiate between patients with stroke and those with TIA (sensitivity of 73% and specificity of 80%). sNfL concentration significantly correlated with cerebral infarction volume (r = .413, P= <.001), this association remained significant after adjusting for established predictors (P= .019). Patients with AIS due to cardioembolism or large artery atherosclerosis had the highest sNfL concentrations. NIHSS on admission (r = .343, P = <.001) and mRS scores after 3 months (r = .306, P = .004) correlated with sNfL concentration, however functional outcome 3 months after stroke was not associated with sNfL after adjusting for potential confounders. CONCLUSIONS: Cases with stroke were distinguishable from those with TIA following the determination of sNfL in the blood samples. The presence and amount of axonal damage estimated by sNfL correlated with the final cerebral infarction volume but was not predictive of degree of disability.