Our previous study had confirmed that lifetime intellectual cognitive reserve (LICR) is associated with better late-life cognition. However, whether LICR can delay cognitive decline remains unknown. We systematically examined the influence of LICR on cognitive trajectories, as well as mild cognitive impairment (MCI) risk, and whether such associations differ by sex. A total of 1308 cognitively intact individuals (mean age 65.54 years) were included. Information on early educational attainment, midlife occupational complexity and mental leisure activities after retirement collected at baseline was used to construct LICR, while cognitive domain scores were derived from several neuropsychological tests assessed at baseline and twice follow-up, using confirmatory factor analysis. Data were analyzed using linear mixed-effects models and Cox regression models. Compared to participants with lower LICR, those with higher LICR exhibited significantly slower language ability decline (β = 0.071, 95

BACKGROUND:As limited medical interventions proved efficacy in intracerebral hemorrhage (ICH), the mechanisms underlying primary and secondary tissue injury remain poorly understood based on hematoma. In this study, we aimed to investigate the transcriptional profiles of immune cells from hematoma samples derived from ICH patients, which was rarely focused before. METHODS:Single cell RNA sequencing (scRNA-seq) was performed on hematoma and blood samples derived from ICH patients, with blood samples from healthy volunteers serving as a control. Subsequent comprehensive analyses, including cell-cell communication and trajectory inference, were conducted to provide a detailed understanding of immune cell characteristics in ICH. RESULTS:Hematoma and blood samples were derived from four ICH patients, with blood samples from three healthy volunteers as control. At the single-cell level, three major immune cell types were identified, with neutrophils playing a predominant role. Subtypes of these immune cells were further characterized based on their profiles in hematoma and blood samples. The role of Toll-like receptor 4 in hematoma in ICH was further investigated from the perspective of immune inflammation and metabolism. CONCLUSION:This study offers a comprehensive overview of the immune cell landscape in ICH, derived from hematoma and blood samples, which has been rarely reported. The dynamic inflammatory processes involving distinct immune cell types were further elucidated, and provides potential therapeutic targets for future interventions.

Cerebral amyloid angiopathy (CAA) is a common small vessel disease characterized by Aβ deposition in cortical and leptomeningeal arteries, leading to lobar intracerebral hemorrhage and vascular cognitive impairment. Despite advances in diagnosis, prognosis remains highly heterogeneous, encompassing risks of recurrent hemorrhage and progressive cognitive decline. This review summarizes recent developments in imaging and fluid biomarkers for prognostic stratification in CAA. Imaging markers, including advanced MRI and molecular PET techniques, have evolved from traditional hemorrhagic indicators, such as cerebral micro-bleeds (CMBs) and cortical superficial siderosis (cSS), to non-hemorrhagic including white matter hyper-intensities (WMHs), and enlarged perivascular spaces (ePVS), which sensitively capture microstructural damage after using quantitative measures. Fluid biomarkers provide dynamic insights into vascular and neuronal injury, including altered plasma Aβ42/Aβ40 ratios, MMPs/TIMPs balance, and elevated neuro-filament light chain (NfL) and glial fibrillary acidic protein (GFAP) levels. Integrating these multi-modal indicators may enable individualized prediction of hemorrhagic and cognitive outcomes and inform precision management strategies. Future research should standardize quantification methods and validate multi-modal models across diverse CAA phenotypes to advance toward personalized prognostic frameworks.

Post-stroke cognitive impairment (PSCI) reflects vulnerability to cognitive decline beyond acute brain injury. Lipoprotein(a) (Lp(a)) is a genetically determined vascular risk factor with pro-inflammatory and pro-atherogenic properties, but the pathways linking Lp(a) to cognitive outcomes after stroke remain unclear. We examined whether systemic inflammation mediates or modifies Lp(a)-related cognitive risk after ischemic stroke. We analyzed data from a prespecified substudy of the Third China National Stroke Registry. Baseline serum Lp(a) and high-sensitivity C-reactive protein (hs-CRP) were measured. PSCI was defined as a Montreal Cognitive Assessment score ≤ 22 at 1 year. Multivariable logistic regression, interaction, joint exposure, and causal mediation analyses were performed to evaluate the role of systemic inflammation in the Lp(a)–PSCI association. Among 954 patients with acute ischemic stroke, higher baseline Lp(a) was associated with increased PSCI risk after adjustment for baseline cognitive performance and clinical covariates (highest vs. lowest tertile: OR, 1.479; 95

BACKGROUND:Although the clinical significance of lipidemic profiles has been reported in ischemic stroke, fewer studies reported the clinical significance of these lipidemic profiles in intracerebral hemorrhage. This study aimed to investigate the relationship between high-density lipoprotein to low-density lipoprotein ratios and long-term clinical outcomes including functional dependence and mortality. METHODS:Based on a multicenter, real-world registry, our study included patients with intracerebral hemorrhage hospitalized within 72 hours from symptoms onset. Divided into quartiles (Q1-Q4), the association between high-density lipoprotein to low-density lipoprotein ratios and poor functional outcomes (modified Rankin Scale scores 3-6) was investigated using multivariable logistic regression models. RESULTS:The final study included 869 intracerebral hemorrhage patients, with a median National Institutes of Health Stroke Scale score of 9 (3-16) and median hematoma volume of 13.4 mL (5.7-31). In the fully adjusted logistic model, where the high-density lipoprotein to low-density lipoprotein ratio was analyzed as a continuous variable, a higher ratio was significantly associated with an elevated odds of poor functional outcome at 90 days (adjusted odds ratio (OR), 4.57 [95% CI 1.70-12.29], P=0.003) and at 1 year (adjusted OR, 2.93 [95% CI 1.08-7.99], P=0.036). The sensitivity analyses confirmed that, compared with high-density lipoprotein or low-density lipoprotein separately, the high-density lipoprotein to low-density lipoprotein ratios emerged as a more robust and consistent predictor in patients with intracerebral hemorrhage without receiving surgical intervention. CONCLUSIONS:Our study delineated the association between high-density lipoprotein to low-density lipoprotein ratios and poor functional outcomes in patients with intracerebral hemorrhage.

Central nervous system involvement by chronic lymphocyte leukemia (CNS-CLL) without Richter transformation is a rare and hard-to-diagnose condition. Nonspecific symptoms and the need for a brain biopsy complicate diagnosis. We report a 58-year-old male with Rai stage 0 CLL who had severe neurological signs. His initial MRI suggested autoimmune-related demyelinating disease. However, high-dose steroids and intravenous immunoglobulin (IVIG) did not help. His neurological status continued to worsen. A multidisciplinary team used advanced imaging (PET-CT showing a hypermetabolic lesion with SUVmax 8.2) and stereotactic brain biopsy. Immunoglobulin heavy chain (IGH) gene clonal rearrangement showed identical clones (IGHV3-64*01/02/07) in both cerebral tissue and bone marrow. This confirmed CNS-CLL. Treatment with ibrutinib stabilized the disease and led to partial cognitive recovery. The patient survived five years without progression. This case and a literature review show that CNS-CLL can have atypical imaging and occur even in early-stage disease. Under targeted therapy, this rare condition may have a better prognosis than previously reported. The report highlights the importance of molecular studies for diagnosis and recommends a multidisciplinary diagnostic approach.

Key point:IRM appears promising and well tolerated as first-line therapy for newly diagnosed PCNS DLBCL in a small pilot cohort; these hypothesis-generating results require confirmation in larger prospective studies. Background:Primary diffuse large B-cell lymphoma of the central nervous system (PCNS DLBCL) is a rare, aggressive lymphoma with rising incidence in elderly patients. Bruton tyrosine kinase (BTK) inhibitors show promise in recurrent/refractory cases, warranting exploration in newly diagnosed disease. Methods:This single-center pilot study evaluated the safety/efficacy of ibrutinib, rituximab, and high-dose methotrexate (IRM) in nine newly diagnosed PCNS DLBCL patients (2018-2019). Treatment included 4 cycles of IRM induction, consolidation (HSCT or 2 additional IRM cycles), and maintenance therapy (ibrutinib/lenalidomide). Results:After induction, overall response rate (ORR) was 100% (complete response [CR]: 77.8%, partial response [PR]: 22.2%). Post-consolidation, CR increased to 88.9%. At a median follow-up of 77.6 months, 5-year overall survival (OS) and progression-free survival (PFS) rates were both 77.8%, with 8 patients in sustained CR and one progression. No treatment-related deaths occurred; grade ≥3 adverse events were rare (2 neutropenia, 2 anemia, 1 gastrointestinal bleeding). Conclusion:In this small pilot cohort, IRM showed promising activity and tolerability as first-line therapy for PCNS DLBCL. These descriptive findings warrant confirmation in larger prospective trials (#ChiCTR1900027811).

Background Atrial fibrillation (AF) pattern, relevant cardiac changes are important predictors of outcomes in AF, but their impact on patients with ischemic stroke and AF remained unclear. We aimed to explore the impact of AF patterns, cardiac structural and functional markers on long-term functional and cognitive outcomes in ischemic stroke patients with AF. Methods Ischemic stroke patients diagnosed with AF were enrolled in this retrospective cohort study. AF pattern was defined by both traditional and novel classification, in which patients were divided into AF diagnosed after stroke (AFDAS) and known before stroke (KAF). Left atrial (LA) diameter, left ventricular ejection fraction (LVEF), natriuretic peptide (BNP) and cardiac troponin (cTnI) were dichotomized according to the median value. Outcomes include poor functional outcome and cognitive impairment at the 1-year follow-up. Multivariable logistic regression was performed to validate the association between AF pattern, parameters of cardiac change and functional and cognitive outcome. Results A total of 377 patients were included. Non-paroxysmal AF patients had a higher risk of poor functional outcome (OR = 3.59, P < 0.0001) and cognitive impairment (OR = 2.38, P = 0.019) than paroxysmal AF patients, while there were no differences between AFDAS and KAF. Lower LVEF (OR = 1.83, P = 0.045) and higher BNP (OR = 2.66, P = 0.001) were associated with poor functional outcome. Lower LVEF (OR = 2.86, P = 0.004), higher LA diameter (OR = 2.72, P = 0.008) and BNP (OR = 2.31, P = 0.023) were associated with cognitive impairment. Conclusions AF type and related cardiac markers can serve as predictors for poor functional and cognitive outcomes. Comprehensive cardiac assessment and monitoring should be strengthened after stroke.

BACKGROUND:Peroxiredoxin 2 (Prx2), an intracellular protein that regulates redox reactions, released from red blood cells is involved in inflammatory brain injury after intracerebral hemorrhage (ICH). Toll-like receptor 4 (TLR4) may be crucial in this process. This study investigated the role of the Prx2-TLR4 inflammatory axis in brain injury following experimental ICH in mice.METHODS:First, C57BL/6 mice received an intracaudate injection of autologous arterial blood or saline and their brains were harvested on day 1 to measure Prx2 levels. Second, mice received an intracaudate injection of either recombinant mouse Prx2 or saline. Third, the mice were co-injected with autologous arterial blood and conoidin A, a Prx2 inhibitor, or vehicle. Fourth, the mice received a Prx2 injection and were treated with TAK-242, a TLR4 antagonist, or saline (intraperitoneally). Behavioral tests, magnetic resonance imaging, western blot, immunohistochemistry/immunofluorescence staining, and RNA sequencing (RNA-seq) were performed.RESULTS:Brain Prx2 levels were elevated after autologous arterial blood injection. Intracaudate injection of Prx2 caused brain swelling, microglial activation, neutrophil infiltration, neuronal death, and neurological deficits. Co-injection of conoidin A attenuated autologous arterial blood-induced brain injury. TLR4 was expressed on the surface of microglia/macrophages and neutrophils and participated in Prx2-induced inflammation. TAK-242 treatment attenuated Prx2-induced inflammation and neurological deficits.CONCLUSIONS:Prx2 can cause brain injury following ICH through the TLR4 pathway, revealing the Prx2-TLR4 inflammatory axis as a potential therapeutic target.

BACKGROUND:Growing evidence suggests that atrial fibrillation (AF) is an independent risk factor for cognitive impairment and dementia, even in the absence of thromboembolic events and stroke. Whether rhythm-control therapy can protect cognitive function remains unclear. We aimed to evaluate the efficacy of rhythm-control strategies in patients with AF regarding cognitive function and dementia risk. METHODS:We systematically searched the PubMed, Embase and Cochrane Library databases for randomised clinical trials, cohort and case-control studies evaluating the associations between rhythm-control strategies and cognitive function outcomes up to May 2023. We assessed the risk of bias using the ROBINS-I and the Cochrane risk-of-bias tool. Both fixed- and random-effects models were used to create summary estimates of risk. RESULTS:We included a total of 14 studies involving 193,830 AF patients. In the pooled analysis, compared with rate-control, rhythm-control therapy was significantly associated with a lower risk of future dementia (hazard ratio (HR) 0.74; 95% confidence interval (CI) 0.62-0.89; I2 = 62%). Among the rhythm-control strategies, AF ablation is a promising treatment that was related to significantly lower risks of overall dementia (HR 0.62; 95% CI 0.56-0.68; I2 = 42%), Alzheimer's disease (HR 0.78; 95% CI 0.66-0.92; I2 = 0%) and vascular dementia (HR 0.58; 95% CI 0.42-0.80; I2 = 31%). Pooled results also showed that compared with patients without ablation, those who underwent AF ablation had significantly greater improvement in cognitive score (standardized mean difference (SMD) 0.85; 95% CI 0.30-1.40; P = 0.005; I2 = 76%). CONCLUSIONS:Rhythm-control strategies, especially ablation, are effective in protecting cognitive function, reducing dementia risk and thus improving quality of life in AF patients.

BACKGROUND:The C-reactive protein-to-albumin ratio (CAR) is a novel prognostic biomarker of systemic inflammation and nutritional status. The association between CAR and the long-term outcome of spontaneous intracerebral hemorrhage (ICH) remains unclear. METHODS:From January 2014 to September 2016, 497 patients with spontaneous ICH were enrolled in our study from 13 hospitals in Beijing. According to the CAR quartiles, patients were classified into four groups (Q1-Q4). Logistic regression was applied to analyze the relationship between different CAR levels and main outcome (90-day and 1-year mRS 4-6). Restricted cubic splines and receiver operating characteristic (ROC) curves of CAR for poor clinical outcomes were assessed. RESULTS:In the multivariate logistic regression model, compared with the lowest quartile of CAR, the adjusted odds ratios of the Q2, Q3, and Q4 group for 90-day mRS score of 4-6 were 3.64 (1.61-8.23), 3.83 (1.67-8.77), and 8.91 (3.85-20.64). In terms of 1-year mRS score of 4-6, compared with the lowest quartile of CAR, the adjusted odds ratios of the Q3 and Q4 group were 3.31 (1.33-8.22) and 6.87 (2.81-16.78). CONCLUSIONS:A high CAR level was associated with a high risk of long-term adverse prognosis in patients with ICH, and the risk of ICH poor outcome increased steadily with CAR rising in a certain range, and maintained in a high level thereafter.

Background and objectives Prior evidence suggests that atrial fibrillation detected after stroke (AFDAS) is distinct from known atrial fibrillation (KAF), with particular clinical characteristics and impacts on outcomes in ischaemic stroke. However, the results remained inconsistent in ischaemic stroke, and the role of AFDAS in haemorrhagic stroke remains unclear. Therefore, we aimed to estimate the prevalence, risk factors and prognostic value of AFDAS in haemorrhagic stroke in comparison with ischaemic stroke.Methods This was a multicentre cohort study. Patients who had an ischaemic and haemorrhagic stroke hospitalised in the Chinese Stroke Center Alliance hospitals were enrolled and classified as AFDAS, KAF or sinus rhythm (SR) based on heart rhythm. Univariate and multivariate logistic regression analyses were used to assess the prevalence, characteristics, risk factors and outcomes of AFDAS, KAF and SR in different stroke subtypes.Results A total of 913 163 patients, including 818 799 with ischaemic stroke, 83 450 with intracerebral haemorrhage (ICH) and 10 914 with subarachnoid haemorrhage (SAH), were enrolled. AFDAS was the most common in ischaemic stroke. There were differences in the risk factor profile between stroke subtypes; older age is a common independent risk factor shared by ischaemic stroke (OR 1.06, 95% CI 1.06 to 1.06), ICH (OR 1.08, 95% CI 1.07 to 1.09) and SAH (OR 1.07, 95% CI 1.05 to 1.10). Similar to KAF, AFDAS was associated with an increased risk of in-hospital mortality compared with SR in both ischaemic stroke (OR 2.23, 95% CI 1.94 to 2.56) and ICH (OR 2.84, 95% CI 1.84 to 4.38).Discussion There are differences in the prevalence, characteristics and risk factors for AFDAS and KAF in different stroke subtypes. AFDAS was associated with an increased risk of mortality compared with SR in both ischaemic stroke and ICH. Rhythm monitoring and risk factor modification after both ischaemic and haemorrhagic stroke are essential in clinical practice. More emphasis and appropriate treatment should be given to AFDAS.

Focal Cortical Dysplasia (FCD) is a frequent cause of drug-resistant focal epilepsy in children and young adults. The international FCD classifications of 2011 and 2022 have identified several clinico-pathological subtypes, either occurring isolated, i.e., FCD ILAE Type 1 or 2, or in association with a principal cortical lesion, i.e., FCD Type 3. Here, we addressed the DNA methylation signature of a previously described new subtype of FCD 3D occurring in the occipital lobe of very young children and microscopically defined by neuronal cell loss in cortical layer 4. We studied the DNA methylation profile using 850 K BeadChip arrays in a retrospective cohort of 104 patients with FCD 1 A, 2 A, 2B, 3D, TLE without FCD, and 16 postmortem specimens without neurological disorders as controls, operated in China or Germany. DNA was extracted from formalin-fixed paraffin-embedded tissue blocks with microscopically confirmed lesions, and DNA methylation profiles were bioinformatically analyzed with a recently developed deep learning algorithm. Our results revealed a distinct position of FCD 3D in the DNA methylation map of common FCD subtypes, also different from non-FCD epilepsy surgery controls or non-epileptic postmortem controls. Within the FCD 3D cohort, the DNA methylation signature separated three histopathology subtypes, i.e., glial scarring around porencephalic cysts, loss of layer 4, and Rasmussen encephalitis. Differential methylation in FCD 3D with loss of layer 4 mapped explicitly to biological pathways related to neurodegeneration, biogenesis of the extracellular matrix (ECM) components, axon guidance, and regulation of the actin cytoskeleton. Our data suggest that DNA methylation signatures in cortical malformations are not only of diagnostic value but also phenotypically relevant, providing the molecular underpinnings of structural and histopathological features associated with epilepsy. Further studies will be necessary to confirm these results and clarify their functional relevance and epileptogenic potential in these difficult-to-treat children.

Purpose:Inflammatory response plays essential roles in the pathophysiology of both ischemic stroke and atrial fibrillation (AF). We aimed to investigate whether composite inflammatory markers, including neutrophil to lymphocyte ratio (NLR), lymphocyte-to-monocyte ratio (LMR) and platelet-to-lymphocyte ratio (PLR), can serve as early predictors of short- and long-term outcomes in ischemic stroke patients with AF. Patients and Methods:Ischemic stroke patients with AF were enrolled in this cohort study. The primary outcome was 1-year functional dependence or death (modified Rankin scale (mRS) score 3-6). Secondary outcomes included hemorrhagic transformation (HT) and early neurological deterioration (END, increase in the National Institutes of Health Stroke Scale (NIHSS) ≥4 within 7 days). Partial correlations were performed to assess the correlation between systemic inflammation markers and admission NIHSS scores. Univariate and multivariate logistic analyses were performed to investigate whether systemic inflammatory markers were independent predictors of adverse outcomes. Results:A total of 408 patients were included. Partial correlation analysis revealed statistically significant but weak correlations between the NLR (r = 0.287; P < 0.001), PLR (r = 0.158; P = 0.001) and admission NIHSS score. Compared with patients without HT or END, patients who developed HT or END had higher NLR and PLR, and lower LMR. Patients in the functional dependence or death group had significantly higher NLR and PLR, and lower LMR than those in the functional independence group (all P < 0.001). Multivariate logistic analysis indicated that NLR, LMR and PLR were independent predictors of HT (OR = 1.069, 0.814 and 1.003, respectively), END (OR = 1.100, 0.768 and 1.006, respectively) and adverse 1-year functional outcome (OR = 1.139, 0.760 and 1.005, respectively). Conclusion:NLR, LMR and PLR were independent predictors for in-hospital HT, END and long-term functional outcome in ischemic stroke patients with AF. Close monitoring of these inflammatory markers may help guide risk stratification and clinical treatment strategies.

Background: Intracerebral hemorrhage (ICH) has high mortality and morbidity rates in the world. Homocysteine (Hcy) has been demonstrated to be an independent risk factor and could predict the prognosis and recurrence of ischemic stroke. In our study, we aimed to find out the relationship between Hcy levels and the severity and prognosis of patients with ICH. Methods: Patients' basic characteristics and laboratory examination results, including the concentration of homocysteine, were taken at baseline from January 2014 to September 2016, and a 1 year follow-up, including the modified Rankin Scale and living status, was taken for all the patients. Logistic regression and Kaplan-Meier survival method were used to analyze the relationship between different Hcy levels and clinical outcome. Results: A total of 551 patients with acute ICH from 13 hospitals in Beijing were enrolled in our study. High Hcy was detected in 284 patients (51.5%). Percentage of male, smoking, drinking, and concentration of hemoglobin A1c and triglyceride levels showed a significant difference between different Hcy level groups (all P-values <0.05). In the logistic regression analysis, high Hcy level is an independent risk factor for the prevalence of 3 month poor prognosis [odd ratio (95% confidence interval) = 1.601 (1.063-2.412), P = 0.0242], especially in female subgroup. In the 1 year follow-up period, high Hcy level patients had a significantly higher rate of fatal incidence compared to normal Hcy level patients (P = 0.0023). Conclusions: High Hcy level was independently associated with poorer 3 month prognosis and a lower survival rate within 1 year in patients with ICH.

目的 探讨原始脑出血评分(original?intracerebral?hemorrhage?scale,OICH)、脑出血分级量表(ICH-grading?scale,ICH-GS)、脑出血功能结局量表(ICH?functional?outcome?score,ICH-FOS)、改良急诊脑出血评分量表(modified?emergency?department?intracerebral?scale,MEDICH)及超早期血肿生长速度(ultraearly?hematoma?growth,uHG)对脑出血患者短期死亡风险的预测价值.方法 收集2014年1月—2016年9月脑出血登记研究中急性脑出血患者的一般临床资料、既往病史、入院后首次实验室检查结果、血压、脑出血部位、血肿体积、住院期间并发症情况.对患者进行发病30?d随访,根据全因死亡情况,将患者分为死亡组和存活组,比较两组间基线资料、uHG(基线血肿体积/发病到基线CT的时间)和不同脑出血评分.通过单因素logistic回归分析判断不同脑出血评分对患者30?d生存结局的影响,进一步通过生存曲线的AUC比较不同评分及联合uHG对30?d死亡的预测效能.结果 研究共纳入脑出血患者1664例,30?d随访死亡308例,存活1356例.单因素logistic回归分析显示,死亡组的OICH、ICH-GS、ICH-FOS、MEDICH各项得分及uHG均高于存活组,差异具有统计学意义.根据出血部位、性别、年龄、出血量进行亚组分析,除幕下出血组外,其余亚组的uHG与30?d死亡均相关(均P<0.05).计算AUC发现,ICH-FOS对患者短期死亡结局的预测价值最高,AUC=0.8599.分析uHG联合ICH-FOS的预测价值,发现对患者结局预测价值较单独ICH-FOS的效能更高(按照uHG是否大于本研究中均值分别赋值0和1,与ICH-FOS其他指标联合构成脑出血功能结局量表-血肿生长速度评分1,AUC=8604;按照uHG四分位数区间分别赋值0、1、2、3,与ICH-FOS其他指标联合构成脑出血功能结局量表-血肿生长速度评分2,AUC=0.8652).结论 不同的常见脑出血预后评分与急性脑出血患者短期生存结局均明显相关且均有较好的预测效能.Uhg联合ICH-FOS评分对脑出血患者短期生存结局较单独ICH-FOS评分具有更高的预测价值.

AbstractObjectiveOur study aimed to investigate the association between the subarachnoid extension of intracranial hemorrhage (SAHE) and clinical outcomes in patients with supratentorial intracerebral hemorrhage (ICH).MethodsWe analyzed the data from a prospective, multi-center, and registry-based database. Two experienced investigators independently assessed ICH imaging data. We compared baseline characteristics and follow-up outcomes. Multivariable logistic regression analysis was used to evaluate the association between SAHE and poor clinical outcomes. We also performed Kaplan–Meier curves and Cox proportional hazards regression analyses to analyze whether SAHE was relevant to a higher mortality rate.ResultsA total of 931 patients were included in this study (SAHE vs. no SAHE, 121 [13.0%] vs. 810 [87.0%]). Patients with SAHE had more severe neurological deficits, higher scores of the mRS, and more remarkable mortality rates at follow-up (allpvalues < 0.05). In multivariable-adjusted models, SAHE was independently associated with a higher risk of poor outcomes (adjusted OR [95%CI]: 2.030 [1.142–3.608] at 3 months; 2.348 [1.337–4.123] at 1 year). In addition, SAHE remained an independent association with an increased death rate at 1 year (adjusted HR [95%CI], 1.314[1.057–1.635]). In the subgroup analysis, the correlation between SAHE and prognosis exists in patients with lobar or deep ICH.ConclusionsSAHE is independently associated with poor outcomes in patients with supratentorial ICH. It may provide a promising target for developing new predictive tools targeting ICH.

Intracerebral hemorrhage (ICH) is one common yet devastating stroke subtype, imposing considerable burdens on families and society. Current guidelines are limited to symptomatic treatments after ICH, and the death rate remains significant in the acute stage. Thus, it is crucial to promote research to develop new targets on brain injury after ICH. In response to hematoma formation, amounts of chemokines are released in the brain, triggering the infiltration of resident immune cells in the brain and the chemotaxis of peripheral immune cells via the broken blood–brain barrier. During the past decades, mounting studies have focused on the roles of chemokines and their receptors in ICH injury. This review summarizes the latest advances in the study of chemokine functions in the ICH. First, we provide an overview of ICH epidemiology and underlying injury mechanisms in the pathogenesis of ICH. Second, we introduce the biology of chemokines and their receptors in brief. Third, we outline the roles of chemokines in ICH according to subgroups, including CCL2, CCL3, CCL5, CCL12, CCL17, CXCL8, CXCL12, and CX3CL1. Finally, we summarize current drug usage targeting chemokines in ICH and other cardio-cerebrovascular diseases. This review discusses the expressions of these chemokines and receptors under normal or hemorrhagic conditions and cell-specific sources. Above all, we highlight the related data of these chemokines in the progression and outcomes of the ICH disease in preclinical and clinical studies and point to therapeutic opportunities targeting chemokines productions and interactions in treating ICH, such as accelerating hematoma absorption and alleviating brain edema.

The aim of this study was to compare the therapeutic effects of non-navigated freehand minimally invasive aspiration and conservative medical care in patients with deep supratentorial intracerebral hemorrhage (ICH). We analyzed data from a prospective multicenter cohort study. Propensity score matching was performed to adjust for possible confounding factors. A total of 122 patients with first-onset deep supratentorial ICH with a volume ≥ 20 ml were enrolled. All patients were followed up at 30 days, 90 days, and 1 year. The mortality rate, functional outcomes, complications, and treatment costs were compared between the two groups. After propensity score matching, 122 patients with a mean age of 56.0 years were included, 77.9