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Abstract Background Chronic subdural hematomas (CSDHs) are one of the most common neurosurgical conditions. The standard surgical technique includes burr-hole craniostomy, followed by intraoperative irrigation and placement of subdural closed-system drainage. The drainage is generally removed after 48 h, which can be described as fixed-time drainage strategy. According to literature, the recurrence rate is 5–33% with this strategy. In our retrospective study, postoperative hematoma volume was found to significantly increase the risk of recurrence. Based on these results, an exhaustive drainage strategy is conducted to minimize postoperative hematoma volume and achieve a low recurrence rate and good outcomes. Methods This is a prospective, multicenter, open-label, blinded endpoint randomized controlled trial designed to include 304 participants over the age of 18–90 years presenting with a symptomatic CSDH verified on cranial computed tomography or magnetic resonance imaging. Participants will be randomly allocated to perform exhaustive drainage (treatment group) or fixed-time drainage (control group) after a one-burr hole craniostomy. The primary endpoint will be recurrence indicating a reoperation within 6 months. Discussion This study will validate the effect and safety of exhaustive drainage after one-burr hole craniostomy in reducing recurrence rates and provide critical information to improve CSDH surgical management. Trial registration Clinicaltrials.gov, NCT04573387. Registered on October 5, 2020.

Background: The optimal treatment for intracranial pseudoaneurysm is unclear. This study aims to analyze the outcome of treating intracranial pseudoaneurysm with a novel covered stent.Materials and Methods: The institutional imaging and clinical databases were retrospectively reviewed for patients with intracranial pseudoaneurysms treated with Willis covered stent from January 2017 to December 2019. The clinical presentations, etiology, intraoperative complications, and immediate and follow-up outcomes were analyzed.Results: A total of 19 patients with 20 pseudoaneurysms were enrolled for analysis. Seventeen patients presented with vision loss and two with epistaxis. Nineteen Willis covered stents were used with one for each patient without technical failure. Intraoperative thrombosis was encountered in one patient (5.3%), which was recanalized by tirofiban. During clinical follow-up, no further epistaxis occurred, and visual acuity improved in three (17.6%) patients. Endoleak occurred in seven (36.8%) patients after the initial balloon inflation and persisted in one (5.3%) patient after balloon re-inflation. This endoleak disappeared at 8 month follow-up. Finally, during angiographic follow-up (median 13 months), parent artery occlusion and in-stent stenosis occurred in one (5.3%) patient. No stent-related ischemic event was encountered.Conclusions: The Willis covered stent is feasible, safe, and efficient in treating intracranial pseudoaneurysms.

Abstract Background Following stroke, microglia can be driven to the “classically activated” pro-inflammatory (M1) phenotype and the “alternatively activated” anti-inflammatory (M2) phenotype. Salidroside (SLDS) is known to inhibit inflammation and to possess protective effects in neurological diseases, but to date, the exact mechanisms involved in these processes after stroke have yet to be elucidated. The purpose of this study was to determine the effects of SLDS on neuroprotection and microglial polarization after stroke. Methods Male adult C57/BL6 mice were subjected to focal transient cerebral ischemia followed by intravenous SLDS injection. The optimal dose was determined by evaluation of cerebral infarct volume and neurological functions. RT-PCR and immunostaining were performed to assess microglial polarization. A transwell system and a direct-contact coculture system were used to elucidate the effects of SLDS-induced microglial polarization on oligodendrocyte differentiation and neuronal survival. Results SLDS significantly reduced cerebral infarction and improved neurological function after cerebral ischemia. SLDS treatment reduced the expression of M1 microglia/macrophage markers and increased the expression of M2 microglia/macrophage markers after stroke and induced primary microglia from M1 phenotype to M2 phenotype. Furthermore, SLDS treatment enhanced microglial phagocytosis and suppressed microglial-derived inflammatory cytokine release. Cocultures of oligodendrocytes and SLDS-treated M1 microglia resulted in increased oligodendrocyte differentiation. Moreover, SLDS protected neurons against oxygen glucose deprivation by promoting microglial M2 polarization. Conclusions These data demonstrate that SLDS protects against cerebral ischemia by modulating microglial polarization. An understanding of the mechanisms involved in SLDS-mediated microglial polarization may lead to new therapeutic opportunities after stroke.