The CSA Cerebral Hemorrhage Minimal Invasive Treatment Society was successfully established in Wuhan, Hubei, China. During the inauguration, the first committee of the CSA Cerebral Hemorrhage Minimal Invasive Treatment Society was established.

Inauguration & 1st Annual Conference of CSA Cerebral Hemorrhage Minimal Invasive Treatment Society was successfully held at China Optics Valley Convention & Exhibition Center in Wuhan, Hubei, Chian. During the conference, many well-known neurology experts in China conducted in-depth discussions on the research progress of minimal invasive treatment of cerebral hemorrhage, which benefited the participants a lot.

Sixty-three patients admitted to 5 hospitals in 2014–2020 for the treatment of severe hypertensive brainstem hemorrhage by CT-guided and bone marker-oriented transcerebellar aspiration were enrolled in this study. The puncture accuracy, duration of hematoma removal, tracheal decannulation, postoperative complications, postoperative consciousness recovery time, Glasgow Outcome Scale (GOS) score, and prognosis outcome at follow-up were retrospectively analyzed. Additionally, the relationship between admission Glasgow Coma Scale (GCS) score and GOS score, and between hematoma volume and prognosis of patients was analyzed at follow-up. Results showed that CT localization–based and bone marker oriented transcerebellar hematoma aspiration in the treatment of severe hypertensive brainstem hemorrhage ensures high puncture accuracy, relatively low surgery risk, and good prognosis. The prognosis relates to the state of consciousness and hematoma volume.

Intracerebral hemorrhage (ICH) is the most disabling form of stroke, but effective treatment protocols for ICH are still limited. The minimally invasive surgery (MIS) is a potential and effective treatment for ICH in recent years. However, it is associated with a risk of rebleeding. This review aims to discuss some key facts about rebleeding, such as thrombolytic agents, therapeutic time window, and first aspiration volume.

Pronounced inflammation after intracerebral hemorrhage (ICH) contributes to secondary brain injury, which seriously affects the prognosis of ICH patients. Fractalkine (FKN)/CX3CR1 pathway may play an important role in regulating inflammatory reactions after ICH. As resident immunocyte in brain, microglia is essential for inflammatory reactions in central nervous system. This study intends to explore the effect of FKN/CX3CR1 pathway on microglia after experimental ICH and its possible mechanisms. In mouse ICH models, FKN and TGF-β1 levels gradually increased and showed a positive correlation, both of which peaked at the third day after ICH model. Compared with ICH only, the ratio of s-FKN/m-FKN, microglia activation, and neuronal apoptosis were all decreased after injecting ADAM10 inhibitor (G1254023X) into the lateral ventricle. The expression of inflammatory factors were increased after stimulation with hemin in BV2 cells. The addition of m-FKN reduced the inflammatory response to a certain extent, and the inhibitor of TGF-β1 could counteract the effect of m-FKN.

In conclusion, in mouse ICH model, the expression of FKN is increased, and m-FKN may inhibit the activation of microglia and reduce neuron apoptosis by promoting the expression of TGF-β1.