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Background and Purpose: Silent brain infarct (SBI), which has traditionally been considered clinically silent, has been proposed as a subclinical risk marker for future cognitive function decline.Methods: We conducted a systematic review of literature in the Cochrane Library, MEDLINE, EMBASE, and the China National Knowledge Infrastructure database.Results: In the end, 19 case-control studies, comprising 6712 participants, and 3 prospective cohort studies comprising 4433 participants, met all inclusion criteria and were included in the systematic review. Meta-analysis of 9 studies showed that SBI was an important factor in cognitive function decline (Mini-Mental State score) (standardized mean difference -.47, 95% confidence interval; -.72 to -.22). Another meta-analysis of 4 studies reported the SBI was an independent factor in cognitive dysfunction (Montreal Cognitive Assessment Scale) (standardized mean difference -3.36, 95% confidence interval; -5.90 to -.82). Ten studies further reported that SBI was associated with decreases in specific areas of cognitive function.Conclusions: These results suggest that rather than being clinically silent, SBI might be a factor inducing cognitive dysfunction. [ABSTRACT FROM AUTHOR]

Highlights • We reviewed the relationship and characteristics between NMO optic neuritis and optic neuritis. • We describe the characteristics of NMO optic nerve and retina pathophysiology. • We highlight the limitations of rodents models of NMO optic neuritis. Abstract Neuromyelitis optica (NMO) and NMO spectrum disorders (NMOSD) have garnered attention due to their high pathogenicity, high risk of relapse, and poor prognosis as an inflammatory central nervous system (CNS) syndrome. There is a consensus that the anti-aquaporin-4 antibody (AQP4-IgG) is the main pathogen detectable in majority of NMOSD patients, including traditional NMO and AQP4-IgG-positive optic neuritis. In serum-negative NMOSD patients, myelin oligodendrocyte glycoprotein (MOG) antibodies are considered pathogenic factors. At present, patients with NMO optic neuritis (NMO-ON) hardly benefit from common therapies. A limitation of studies on NMO-ON is the inadequacy of animal models. This review article focuses on the characteristics of visual impairments in NMOSD and the application of experimental rodent models which are required for elucidating the pathology and potential treatments for NMO visual impairment. [ABSTRACT FROM AUTHOR]

• Seizure risk after stroke mechanic thrombectomy and thrombolysis was compared. • Incidence of post-stroke seizures did not differ between the two methods. • Mechanic thrombectomy is associated with lower risk of early onset of seizure. • Late-onset seizure risk did not differ significantly between thrombolytic methods. We conducted a systematic review and meta-analysis to evaluate the risk of early and late onset seizures following stroke mechanic thrombectomy (MT) compared with other systematic thrombolytic strategies. A literature search was conducted to identify articles covering databases (PubMed, Embase, and Cochrane Library) published from 2000 to 2022. The primary outcome was the incidence of post-stroke epilepsy or seizures following MT or in combination with intravenous thrombolytics therapy. Risk of bias was assessed by recording study characteristics. The study was conducted according to the PRISMA guidelines. There were 1346 papers in the search results, and 13 papers were included in the final review.We identified 29,793 patients with stroke, of which 695 had seizures. Pooled incidence of post-stroke seizures had no significant difference between mechanic thrombolytic group and other thrombolytic strategy group (OR=0.95 (95%CI= 0.75-1.21); Z=0.43; p=0.67). In subgroup analysis, mechanic group have a lower risk of post-stroke early onset of seizures (OR=0.59 (95%CI=0.36-0.95); Z=2.18; p<0.05) but showed no significant difference in post-stroke late onset of seizures (OR=0.95 (95%CI= 0.68-1.32); Z=0.32; p=0.75). MT may be associated with a lower risk of post-stroke early onset of seizures, despite MT does not affect the pooled incidence of post-stroke seizures compared with other systematic thrombolytic strategies. [ABSTRACT FROM AUTHOR]

Objective: This study examined the clinical features, functional outcomes, and prognostic indicators of acute ischemic stroke (AIS) patients who had an Alberta Stroke Program Early Computed Tomography Score (ASPECTS) ≤ 5 and who underwent mechanical thrombectomy (MT).Methods: We included consecutive AIS patients with ASPECTS ≤ 5 who had received MT at the same hospital. Demographic, clinical, and radiological data were collected and analyzed. Functional outcome at 90 days after treatment was classified as good or poor based on the modified Rankin Scale (mRS).Results: Of the 152 included patients with ASPECTS ≤ 5 who received MT, 64 (42.11%) experienced poor functional outcomes and 32 (21.1%) experienced good functional outcomes. The independent predictors of poor functional outcomes were the presence of respiratory tract infections (OR 3.72, 95% CI 1.17-11.91), modified thrombolysis in cerebral infarction (OR 0.41, 95% CI 0.2-0.83), symptomatic intracerebral hemorrhage (sICH) (OR 4.96, 95% CI 1.36-18.13), and baseline score on the National Institute of Health Stroke Scale (NIHSS) (OR 1.18, 95% CI 1.03-1.36). Independent predictors of 90-day mortality included time from groin puncture to recanalization (OR 1.03, 95% CI 1.01-1.05), NIHSS scores (OR 1.28, 95% CI 1.12-1.47) and the occurrence of sICH (OR 1.81, 95% CI 1.25-5.75).Conclusion: AIS patients with ASPECTS ≤ 5 can experience good functional outcomes after MT. However, patients with sICH, respiratory infection, higher NIHSS score or failed recanalization are more likely to experience poor functional outcomes. [ABSTRACT FROM AUTHOR]

Research has shown that cerebral ischemia-reperfusion injury (CIRI) involves a series of physiological and pathological mechanisms, including inflammation, oxidative stress, and cell apoptosis. The cannabinoid receptor 2 agonist AM1241 has been found to have anti-inflammatory and anti-oxidative stress effects. However, it is unclear whether AM1241 has a protective effect against brain ischemia-reperfusion injury, and its underlying mechanisms are not yet known. In this study, we investigated the anti-inflammatory, anti-oxidative stress, and anti-apoptotic effects of AM1241 and its mechanisms in BV2 cells stimulated with H 2 O 2 and in a C57BL/6 mouse model of CIRI in vitro and in vivo , respectively. In vitro , AM1241 significantly inhibited the release of pro-inflammatory cytokines TNF-α and IL-6, reactive oxygen species (ROS), and the increase in Toll-like receptor 4/myeloid differentiation protein 2 (MD2/TLR4) complex induced by H 2 O 2. Under H 2 O 2 stimulation, MD2 overexpression resulted in increased levels of MD2/TLR4 complex, TNF-α, IL-6, NOX2, BAX, and Cleaved-Caspase3 (C-Caspase3), as well as the activation of the MAPK pathway and NF-κB, which were reversed by AM1241. In addition, molecular docking experiments showed that AM1241 directly interacted with MD2. Surface Plasmon Resonance (SPR) experiments further confirmed the binding of AM1241 to MD2. In vivo , AM1241 significantly attenuated neurofunctional impairment, brain edema, increased infarct volume, oxidative stress levels, and neuronal apoptosis in CIRI mice overexpressing MD2. Our study demonstrates for the first time that AM1241 alleviates mouse CIRI by inhibiting the MD2/TLR4 complex, exerting anti-inflammatory, anti-oxidative stress and anti-apoptotic effects. [Display omitted] • AM1241 protects against cerebral ischemia-reperfusion injury (CIRI). • MD2 promotes microglial inflammation, oxidative stress, and apoptosis. • In microglia, AM1241 exerts anti-inflammatory, antioxidant, and anti-apoptotic effects by inhibiting MD2/TLR4. • AM1241 can directly bind to and interact with MD2. [ABSTRACT FROM AUTHOR]

High-mobility group box 1 (HMGB1) and advanced glycation end-products (RAGE) are potential mediators of inflammation. We investigate the association between levels of HMGB1 and soluble RAGE (sRAGE) following intracerebral hemorrhage (ICH) and the severity of ICH. There was a significant trend towards higher poor functional outcome rate with increasing HMGB1 and sRAGE tercile. The correlation analysis indicated that the levels of HMGB1and sRAGE were positively correlated with hematoma volume. The receiver operating curve (ROC) was 0.718 for HMGB1 and 0.631 for sRAGE to poor functional outcome. HMGB1 and sRAGE quantification provides more accurate prognostic information after ICH. Unlabelled Image • Patients with poor functional outcome had higher levels of HMGB1 and sRAGE. • There was a significant trend towards higher poor functional outcome rate with increasing HMGB1 and sRAGE tercile. • The AUCs were generated to examine the ability of HMGB1 and sRAGE to predict clinical poor outcome. • When the level of HMGB1 was 860 pg/ml, the sensitivity was 81.5% and the corresponding specificity was 71.7%. • When the level of sRAGE was 602 pg/ml, the sensitivity was 70.4% and the corresponding specificity was 62.3%. [ABSTRACT FROM AUTHOR]

Highlights • BBB dysfunction is the main consequence of hemorrhagic transformation and I/R injury. • GAS can reduce the neurobehavioral impairment and restore exploration ability in rats. • GAS treatment can protect against cell death caused by brain injury. Abstract Brain damage, including blood-brain barrier (BBB) dysfunction, neurological behavior deficit, cerebral infarction and inflammation, is commonly caused by ischemic-reperfusion (I/R) injury. Prevention of the above biological process defects is considered beneficial for patient recovery after I/R injury. This study was aimed to assess the neuroprotective effect of Gastrodin (GAS), an herbal agent, in experimentally induced cerebral ischemia. Sprague-Dawley adult rats were randomly divided into six groups: Sham-operated control group (Sham), middle cerebral artery occlusion (MCAO) group, GAS (50, 100, and 200 mg/kg) pretreatment + MCAO groups (GAS) and Nimodipine (NIM) + MCAO, namely, the NIM group. Additionally, an OGD/R model using BV-2 microglia was established in vitro to simulate I/R injury. We showed here that the neurological scores of rats in the GAS groups were significantly improved compared with the MCAO group. Moreover, the area of cerebral infarction in the GAS pretreatment groups and the NIM group was significantly reduced. Furthermore, Evans blue leakage volume was significantly reduced with GAS pretreatment notably at dose 100 mg/kg. Expression of matrix metalloproteinase 2 (MMP2) and MMP9 in GAS groups was markedly decreased when compared with MCAO group. In BV-2 microglia exposed to OGD/R given GAS pretreatment, MMP2 and MMP9 positive cells were reduced in numbers. The present results have shown that GAS pretreatment significantly compensated for neurological behavior defects in rats with I/R-induced injury, reduced brain infarction size, reversed BBB impairment, and attenuated inflammation. It is suggested that pretreatment with GAS before surgery is beneficial during recovery from I/R injury. [ABSTRACT FROM AUTHOR]