Intracerebral hemorrhage (ICH) is a devastating medical emergency with high mortality and severe neurological deficit. ICH-related poor outcomes are due to a combination of pathological processes that could be complicated by secondary insults. TWIK-related K+ channel 1 (TREK-1) is a two-pore-domain potassium channel that is highly expressed in the mammalian nervous system. Previous studies have shown that TREK-1 channels play important roles in various central nervous system diseases. However, its role in the secondary injuries after intracerebral hemorrhage remains unknown. In this study, we explored the function of TREK-1 in secondary blood-brain barrier injuries and neuroinflammation after intracerebral hemorrhage in mice. Adult male TREK-1−/− mice and WT mice were subjected to a collagenase-induced ICH model. Immunostaining, western blot, and enzyme-linked immunosorbent assay were used to assess inflammatory infiltration and neuronal death. Blood-brain barrier compromise was assessed using electron microscopy and Evans Blue dye injection on days 1 and 3 after intracerebral hemorrhage. Magnetic resonance imaging and behavioral assessments were conducted to evaluate the neurologic damage and recovery after intracerebral hemorrhage. Genetic deficiency of TREK-1 channel exacerbated blood-brain barrier impairment and promoted cerebral edema after intracerebral hemorrhage. Meanwhile, TREK-1 deficiency aggravated focal inflammatory featured by the increased recruitment of microglia and neutrophils, the enhanced secretion of proinflammatory factors interleukin-1 beta (IL-1β), tumor necrosis factor alpha (TNF-α), and cell adhesion molecules (CAMs). Furthermore, TREK-1 deficiency promoted neuronal injury and neurological impairment. These results establish the first in vivo evidence for the protective role of TREK-1 in blood-brain barrier injury and neuroinflammation after intracerebral hemorrhage. TREK-1 may thereby be harnessed to a potential therapeutical target for the treatment of intracerebral hemorrhage.

BACKGROUND AND PURPOSE: In clinical practice, stent diameter is one of the variable properties important for endovascular treatment. A consensus guideline for stent retriever size selection has yet to be established. The aim of this study was to investigate the effects of different diameters of Solitaire retrievers on outcomes. MATERIALS AND METHODS: Of 628 patients enrolled from the Endovascular Treatment for Acute Anterior Circulation Ischemic Stroke Registry, 256 were treated with the Solitaire 4-mm device and 372, with the 6-mm device. We matched patients treated with the 2 stent sizes using propensity score analysis. The successful outcome was reperfusion as measured by the modified Thrombolysis in Cerebral Infarction score immediately postprocedure and the dichotomized modified Rankin Scale score at 90 days. Symptomatic intracerebral hemorrhage and in-hospital mortality were also recorded. RESULTS: After propensity score analysis, group outcomes did not differ. In addition, in patients with atherosclerosis-related occlusion, a higher reperfusion rate (P = .021) was observed in the Solitaire 4 group, as well as a shorter time interval (P = .002) and fewer passes (P = .025). Independent predictors of successful reperfusion in patients with atherosclerotic disease on logistic analysis were the small stent (OR, 3.217; 95% CI, 1.129–9.162; P = .029) and the propensity score acting as a covariate (OR, 52.84; 95% CI, 3.468–805.018; P = .004). CONCLUSIONS: We found no evidence of a differential effect of intra-arterial therapy based on the size of Solitaire retrievers. In patients with atherosclerotic disease, favorable reperfusion was associated with deployment of a small stent.

Herein, we evaluated the efficacy and safety of intra-arterial mild hypothermia in combination with arterial thrombolysis to treat acute cerebral infarction due to middle cerebral artery occlusion. A total of 26 patients with acute middle cerebral artery occlusion were divided into a normothermia group (n = 15) and a mild hypothermia group (n = 11). The infarct volumes at 24 h and 7 days after the operation were compared between the normothermia group and the mild hypothermia group. Additionally, we compared neurological deficit scores between the two groups at 24 h, 7 days, and 1 mo after the operation. The infarct volumes and neurological deficit scores of the mild hypothermia group were significantly reduced compared to those in the normothermia group (p < 0.05). Furthermore, no adverse reactions or complications occurred in the mild hypothermia group. Intra-arterial mild hypothermia reduced infarct volume after ischemia–reperfusion injury in the arterial thrombolysis of an acute cerebral infarction. Additionally, it improved the prognosis of patients with an acute middle cerebral artery occlusion, suggesting that this procedure is safe and effective for treating acute cerebral infarction.

Multiple cellular components, including neuronal, glial and endothelial cells, are involved in the sophisticated pathological processes following central nervous system injury. The pathological process cannot reduce damage or improve functional recovery by merely targeting the molecular mechanisms of neuronal cell death after central nerve system injuries. Eph receptors and ephrin ligands have drawn wide attention since the discovery of their extensive distribution and unique bidirectional signaling between astrocytes and neurons. The roles of Eph/ephrin bidirectional signaling in the developmental processes have been reported in previous research. Recent observations suggest that Eph/ephrin bidirectional signaling continues to be expressed in most regions and cell types in the adult central nervous system, playing diverse roles. The Eph/ephrin complex mediates neurogenesis and angiogenesis, promotes glial scar formation, regulates endocrine levels, inhibits myelin formation and aggravates inflammation and nerve pain caused by injury. The interaction between Eph and ephrin is also considered to be the key to angiogenesis. This review focuses on the roles of Eph/ephrin bidirectional signaling in the repair of central nervous system injuries.

BACKGROUND AND PURPOSE: Endovascular thrombectomy has been accepted as the standard of care for patients with acute ischemic stroke. Our aim was to investigate the clinical outcomes of patients with mild ischemic stroke with acute proximal large-vessel occlusion after endovascular treatment within 24 hours of symptom onset. MATERIALS AND METHODS: Between January 2014 and August 2017, ninety-three Chinese patients with mild ischemic stroke (NIHSS scores, 0–8) and large-vessel occlusion with endovascular treatment were retrospectively enrolled from 7 comprehensive stroke centers. They were divided into 2 groups: ≤6 hours and 6–24 hours from symptom onset to groin puncture. We analyzed their modified Rankin Scale scores at 90 days, symptomatic intracranial hemorrhage at 48 hours, and mortality during 90 days. Multivariable linear regression analysis was used to identify predictors for NIHSS shift after discharge. RESULTS: Twenty-nine patients received endovascular treatment within 6–24 hours after symptom onset and had an imaging mismatch based on perfusion CT or diffusion-weighted MR imaging. There were no substantial differences between the 2 groups in 90-day functional independence (P = .54) and the risks of the combination of symptomatic intracranial hemorrhage and death (P = .72). Two significant indicators of NIHSS shift were 48-hour symptomatic intracranial hemorrhage (unstandardized β = 7.28; 95% CI, 3.48–11.1; P < .001) and baseline systolic blood pressure (unstandardized β = 0.08; 95% CI, 0.03–0.14; P = .005). CONCLUSIONS: Patients with mild ischemic stroke and large-vessel occlusion in the anterior circulation, an imaging mismatch, and endovascular treatment within 6–24 hours of initial symptoms showed no heterogeneity in the efficacy and safety outcome compared with those treated ≤6 hours from symptom onset.

This study aimed to assess the risk of death from non-traumatic intracerebral hemorrhage (ICH) using a machine learning model. 1274 ICH patients who met the specified inclusion and exclusion criteria were analyzed retrospectively in the MIMIC IV 3.0 database. Patients were randomly divided into training, validation, and testing datasets in a ratio of 6:2:2 based on the outcome distribution. Data from the Second Hospital of Lanzhou University were used as an external validation set. This study used LASSO regression and multivariable logistic regression analysis to screen for features. We then employed XGBoost to construct a machine-learning model. The model’s performance was evaluated using ROC curve analysis, calibration curve analysis, clinical decision curve analysis, sensitivity, specificity, accuracy, and F1 score. Conclusively, the SHapley Additive exPlanations (SHAP) method was employed to interpret the model’s predictions. Deaths occurred in 572 out of the 1274 ICH cases included in the study, resulting in an incidence rate of 44.9%. The XGBoost model achieved a high AUC when predicting deaths in ICH patients (train: 0.814, 95%CI: 0.784 − 0.844; validation: 0.715, 95%CI: 0.653 − 0.777; test: 0.797, 95%CI: 0.743 − 0.851). The importance of SHAP variables in the model ranked from high to low was: ’GCS motor’, ’Age’, ’GCS eyes’, ’Low density lipoprotein (LDL)’, ’ Albumin’, ’ Atrial fibrillation’, and ’Gender’. The XGBoost model demonstrated good predictive performance in both the validation and external validation datasets. The XGBoost machine learning model we built has demonstrated strong performance in predicting the risk of death from ICH. Furthermore, the SHAP provides the possibility of interpreting machine learning results.