Intracerebral hemorrhage (ICH) is associated with the highest mortality and morbidity despite only constituting approximately 10–15% of all strokes. Complex underlying mechanisms consisting of cytotoxic, excitotoxic, and inflammatory effects of intraparenchymal blood are responsible for its highly damaging effects. Oxidative stress (OS) also plays an important role in brain injury after ICH but attracts less attention than other factors. Increasing evidence has demonstrated that the metabolite axis of hemoglobin‐heme‐iron is the key contributor to oxidative brain damage after ICH, although other factors, such as neuroinflammation and prooxidases, are involved. This review will discuss the sources, possible molecular mechanisms, and potential therapeutic targets of OS in ICH.

Aim: Inflammation plays a role in secondary brain injury after intracerebral hemorrhage (ICH). We aimed to determine the prognostic significance of admission white blood cell (AWC), neutrophil count (ANC), lymphocyte count, monocyte count and neutrophil to lymphocyte ratio (NLR) for 90-day outcome after ICH. Patients & methods: A total of 336 patients with spontaneous ICH were retrospectively investigated. Clinical outcome was assessed by modified Rankin Scale at 90 days. Results: Multivariate analysis showed that higher AWC, ANC, NLR were independently associated with mortality and worse outcome. Moreover, NLR showed a higher predictive ability in mortality than in poor outcome in receiver operating characteristic analysis. Linear regression analyses revealed admission Glasgow Coma Scale score and ICH volume were mostly correlated with these indices. Conclusion: Elevated levels of AWC, ANC and NLR were independently related to poor 90-day outcome after ICH. NLR may be a novel inflammatory biomarker follo...

Intracerebral hemorrhage(ICH) accounts for 10-30% of all types of stroke. Bleeding within the brain parenchyma causes gray matter (GM) destruction as well as proximal or distal white matter (WM) injury (WMI) due to complex pathophysiological mechanisms. Because WM has a distinct cellular architecture, blood supply pattern and corresponding function, and its response to stroke may vary from that of GM, a better understanding of the characteristics of WMI following ICH is essential and may shed new light on treatment options. Current evidence using histological, radiological and chemical biomarkers clearly confirms the spatio-temporal distribution of WMI post- ICH. Although certain types of pathological damage such as inflammatory, oxidative and neuro-excitotoxic injury to WM have been identified, the exact molecular mechanisms remain unclear. In this review, we briefly describe the constitution and physiological function of brain WM, summarize evidence regarding WMI, and focus on the underlying pathophysiological mechanisms and therapeutic strategies.

Erythrocytes undergo certain morphological changes resembling apoptosis during senescence or in an abnormal state/site, which is termed eryptosis. This process is characterized by phosphatidylserine (PS) exposure, membrane blebbing, and cell shrinkage. Eryptotic erythrocytes are subsequently removed via macrophage-mediated efferocytosis. In hemorrhagic stroke (HS), blood within an artery rapidly bleeds into the brain tissue or the subarachnoid space, resulting in severe neurological deficits. A hypoxic, over-oxidative, and pro-inflammatory microenvironment in the hematoma leads to oxidative stress, hyperosmotic shock, energy depletion, and Cl^– removal in erythrocytes, which eventually triggers eryptosis. In addition, eryptosis following intracerebral hemorrhage favors hematoma clearance, which sheds light on a common mechanism of intrinsic phagocytosis. In this review, we summarized the canonical mechanisms of eryptosis and discussed its pathological conditions associated with HS. Understanding the role of eryptosis in HS may uncover additional potential interventions for further translational clinical research.

We sought to perform a network meta-analysis to compare the safety and efficacy of the systemic administration of corticosteroids for the treatment of COVID-19. A Bayesian network meta-analysis was performed to combine the direct and indirect evidence. The surface under the cumulative ranking curve was obtained to estimate the ranking probability of the treatment agents for each outcome. The efficacy outcome was 28-day all-cause mortality. The safety outcome was serious adverse events. A total of 16 trials with 2992 patients comparing four treatments (dexamethasone, hydrocortisone, methylprednisolone, and placebo) were identified. Direct analysis showed that corticosteroids were associated with a reduced risk of 28-day mortality compared with usual care (risk ratio [RR] 0.83; 95% confidence interval [CrI] 0.70-0.99). Network analysis showed that the pooled RR was 0.63 (95% CrI 0.39-0.93) for all-cause mortality at 28 days comparing methylprednisolone with usual care or placebo (surface under the cumulative ranking curve: 91%). Our analysis demonstrated that patients who received a low dose of corticosteroids (RR 0.80; 95% CrI 0.70-0.91) and a long course of treatment (RR 0.81; 95% CrI 0.71-0.91) had higher survival rates than patients in the placebo group. Administration of corticosteroids was associated with a reduced all-cause mortality at 28 days compared with placebo or usual care. Our analysis also confirmed the mortality benefit associated with low-dose and long-term treatment with corticosteroids.