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Peri-ophthalmic aneurysm is a special type of aneurysm. We assessed the relationship between ophthalmic artery (OA) origin and aneurysm and examined the effect of a pipeline embolization device (PED, Covidien/Medtronic) with or without coils on aneurysm occlusion rate and visual outcomes.We retrospectively analyzed 194 peri-ophthalmic aneurysms in 189 patients among 1171 patients treated with a PED in a Chinese post-market multi-center registry study from November 2014 to October 2019. Peri-ophthalmic aneurysms were defined as carotid-ophthalmic segment aneurysms arising from the internal carotid artery dorsal wall at, or distal to, the OA origin, with a superior or superomedial projection. The relationship between OA origin and the aneurysm was classified as follows: type A, OA originating separate from the aneurysm; type B, OA originating from the aneurysm neck or dome. Patients with aneurysm were divided into the PED-only group and the PED + coils group according to treatment.The median follow-up time was 6.8 months (range, 5.3-20.2 months). There were 163 occluded aneurysms (84%) and 31 aneurysms with incomplete occlusion (16%). A multivariate analysis showed that type B aneurysm was a risk factor for incomplete occlusion in the PED-only group (odds ratio [OR] 4.854, 95% confidence interval [CI] 1.878-12.548, P = 0.001). Visual symptoms at final follow-up correlated with preoperative visual symptoms (OR 22.777, 95% CI 3.115-166.555, P = 0.002).Type B aneurysm is associated with a lower occlusion rate after PED-only treatment. Patients with preoperative visual symptoms should be treated promptly to avoid permanent visual symptoms.

Hyperperfusion-induced intracerebral hemorrhage (HICH) is a relatively rare but potentially devastating event after carotid artery stenting (CAS). Staged angioplasty (SAP), a two-stage form of CAS, has been shown to be effective for preventing cerebral hyperperfusion syndrome (CHS). The aim of our retrospective single-center study was to investigate the safety and efficacy of SAP to prevent HICH in patients with very severe carotid stenosis (90%-99%) and poor collateral compensation.One hundred and fifty-three patients with severe symptomatic carotid artery stenosis ≥90% between November 2011 and August 2018, 96 were scheduled to undergo regular CAS and 57 were scheduled for SAP. High risk of HICH were considered based on severe stenosis degree (90%-99%) and poor collateral compensation, which were determined using digital subtraction angiography and qualitative CT perfusion. The patients' clinical, procedural information and occurrence of HICH were compared between regular CAS and SAP groups.Fifty-seven patients scheduled for SAP, 3 of them were switched to regular CAS because of intraoperative dissection. The median interval between stages I and II was 8 days (IQR: 4-20 days). One case who switched to regular CAS suffered from HICH. HICH occurred in one patient (1.75%, 1/57) in the SAP group and 12 patients (12.5%, 12/96) in the regular CAS group (OR: 0.117, 95% CI: 0.014-0.990, p=0.049). Multivariate analysis showed that SAP was negatively related to CHS (OR: 0.117; 95% CI 0.014-0.990; p=0.049).SAP is an effective treatment for avoiding HICH in patients with carotid pre-occlusive stenosis (90%-99%) and poor collateral compensation.

Effective treatment strategies for vertebrobasilar dissecting aneurysms (VBDAs) remain controversial due to their high morbidity and mortality. The aim of the present study was to evaluate the efficacy of overlapping stent-assisted coil embolization (OSCE) in VBDA patients. A total of 42 patients with VBDA were retrospectively examined by OSCE from May 2015 to August 2019. Patients' clinical and radiological parameters were assessed at discharge and during interim follow-up. Safety, technical feasibility and follow-up clinical and imaging observations for therapy were also evaluated retrospectively. The average age of the 42 patients who underwent OSCE was 54 years (range 33 to 74 years). Overlapping stents were successfully implanted in all patients after coil embolism. Overall clinical results were effective (score on a modified Rankin scale from 0 to 2) in all patients. In the meantime, all patients had favorable outcomes when evaluating telephone calls or digital subtractive angiography (DSA) imaging. Among 42 patients, one patient died due to a perioperative rupture. All the remaining 41 patients had a good prognosis during the follow-up telephone call, with a median follow-up of 28 months (range, 2 to 55 months). The total number of DSA recurrences was 20. Subsequent DSA results showed that all aneurysms were completely occluded while in only one case the parent artery of the aneurysm was completely closed. OSCE in VBDAs patients is safe and effective. This technique showed favorable results in clinical and imaging follow-ups for non-ruptured and ruptured VBDAs.

IntroductionSeizures are a common complication that leads to neurological deficits and affects outcomes after aneurysmal subarachnoid haemorrhage (aSAH). However, whether to use prophylactic anticonvulsants in patients with aSAH remains controversial. Our study aims to determine whether short-term (7 days) sodium valproate could prevent seizure occurrence and improve neurological function in patients with SAH caused by anterior circulation aneurysm rupture and treated with clipping.Methods and analysisIn this multicentre randomised evaluator-blind placebo-controlled trial, 182 eligible patients with good-grade aSAH planned for surgical clipping will be enrolled from four neurosurgical centres in China. In addition to standard care, patients will be randomly assigned to receive sodium valproate 20 mg/kg daily or matching placebo. After aneurysmal clipping, patients will be followed up at discharge, 90 days and 180 days. The primary outcomes are the incidence of early and late seizures. The secondary outcomes include aSAH-related complications, sodium valproate-related adverse effects, modified Rankin Scale (mRS) (on discharge, at 90 days, 180 days), rate of good outcome (defined as mRS 0–2), all-cause death (at 90 days, 180 days) and Montreal Cognitive Assessment score (at 180 days). All analyses are by intention-to-treat.Ethics and disseminationThis study will be conducted according to the principles of Declaration of Helsinki and good clinical practice guidelines. This trial involves human participants and has been approved by the ethics committee of West China Hospital. Informed consent will be achieved from each included patient and/or their legally authorised representative. Preliminary and final results from this study will be disseminated through manuscript publishing and international congresses presentations. Any protocol amendments will be approved by the ethics committee of West China Hospital and subsequently updated on ChiCTR.Trial registration numberChiCTR.org identifier: ChiCTR2100050161.

ObjectiveTo analyze the complications and long-term results of endovascular management of vertebrobasilar trunk large (≥10 mm) aneurysms (VBTLAs) and identify predictors of outcomes.MethodsBetween 2014 and 2020, 6,987 patients with intracranial aneurysms were referred to our center for aneurysm management and 2,224 patients have undergone the endovascular procedures. We retrospectively reviewed the database and identify all the patients with VBTLAs.ResultsA total of 62 VBTLAs were identified. The median aneurysm size was 13.4 mm [interquartile range (IQR) 11.5–18.7]. Among them, 24 aneurysms were treated with overlapping stent techniques, 18 aneurysms were treated with flow diversion, 14 aneurysms were treated with single stent-assisted coiling, and 6 aneurysms were treated with coiling alone. Ten patients were treated with parent artery occlusion or unilateral vertebral artery occlusion. Periprocedural complications were occurred in 7 (11.3%) patients. Clinical follow-up was obtained at the median of 27.5 months (IQR 15.3–58.5). The overall complication rate was 16.1% (10/62), including nine ischemic events and one hemorrhagic event. The combined disability and neurological mortality rate was 12.9% (8/62), with 4 (6.5%) deaths. The favorable outcome rate at follow-up was 87.1% (54/62). The complication-free cumulative survival rates at 1 and 5 years were 86.8 and 82.0%, respectively. The overall cumulative survival rates at 1 and 5 year were 96.5 and 89.8%, respectively. In the multivariate Cox regression analysis, longer procedure time (>115 min) (P = 0.037) and ischemic onset (P = 0.005) predict complications. Angiography follow-up was available for 36 patients at the median of 6.0 months (IQR 6–12), with a complete occlusion rate of 77.8% (28/36). Two (5.6%) aneurysms were recanalized and subsequently received the retreatment. Subgroup analysis did not find any differences in the complete occlusion rate between endovascular strategies.ConclusionEndovascular management of VBTLAs has a reasonable safety profile with favorable 5-year cumulative survival rates and imaging outcomes at follow-up. Prolonged procedure and ischemic onset are associated with a high risk of overall complications.

Objective: Peri-ophthalmic aneurysm is a special type of aneurysm. We assessed the relationship between ophthalmic artery (OA) origin and aneurysm and examined the effect of a pipeline embolization device (PED, Covidien/Medtronic) with or without coils on aneurysm occlusion rate and visual outcomes.Methods: We retrospectively analyzed 194 peri-ophthalmic aneurysms in 189 patients among 1,171 patients treated with a PED in a Chinese post-market multi-center registry study from November 2014 to October 2019. Peri-ophthalmic aneurysms were defined as carotid–ophthalmic segment aneurysms arising from the internal carotid artery dorsal wall at, or distal to, the OA origin, with a superior or superomedial projection. The relationship between OA origin and the aneurysm was classified as follows: Type A, OA originating separate from the aneurysm; Type B, OA originating from the aneurysm neck or dome. Patients with aneurysm were divided into the PED-only group and the PED + coils group according to treatment. Results: The median follow-up time was 6.8 months (range, 5.3–20.2 months). There were 163 occluded aneurysms (84%) and 31 aneurysms with incomplete occlusion (16%). A multivariate analysis showed that Type B aneurysm was a risk factor for incomplete occlusion in the PED-only group (odds ratio [OR] 4.951, 95% confidence interval [CI] 1.904-12.875, p = 0.001). Visual symptoms at final follow up correlated with preoperative visual symptoms (OR 16.005, 95% CI 2.505-102.273, p = 0.003).Conclusions: Type B aneurysm is associated with a lower occlusion rate after PED-only treatment. Patients with preoperative visual symptoms should be treated promptly to avoid permanent visual symptoms.

Objective Hyperperfusion-induced intracranial hemorrhage (HICH) is the most frequent cause of death following carotid artery stenting (CAS). This study aimed to identify the presence of HICH after CAS and evaluate demographic and clinical variables associated with HICH. Methods We retrospectively reviewed clinical data of 446 consecutive patients with symptomatic severe carotid stenosis treated with CAS between November 2011 and August 2018. Good collateral compensation was defined as patency of the anterior communicating artery with well-developed bilateral A1 segments with or without posterior communicating arteries, according to the classification of Katano et al. Univariate and multivariate analyses were performed to determine whether there was a correlation between demographic and clinical variables and development of HICH. Results Stent placement was successful in all patients. Of 446 patients, 14 had HICH (3.14%); 1 of 14 (7.14%) patients displayed 80%–90% stenosis, and 13 patients had stenosis ≥90%. Thirteen patients (92.86%) had poor collateral circulation compensation. Two patients (14.3%) died despite rescue efforts. Age (≥70 years), degree of carotid artery stenosis (≥90%), and poor compensation of collateral circulation were associated with a higher frequency of HICH after CAS. Severe carotid artery stenosis (≥90%) was independently associated with HICH after stenting (odds ratio 13.633, P = 0.014). Conclusions The incidence rate of HICH was 3.14%. Patients with severe carotid artery stenosis (≥90%) are at high risk for developing HICH after CAS. Further investigations are needed to better describe the contribution of other risk factors, including poor compensation of collateral circulation (especially anterior circulation).

Background and purpose Mitochondrial dysfunction is involved in the mechanism of early brain injury (EBI) following subarachnoid hemorrhage (SAH). Blood-brain barrier disruption is a devastating outcome in the early stage of SAH. In this study, we aimed to investigate the role of a mitochondria-related drug Mitoquinone (MitoQ) in blood-brain barrier disruption after SAH in rats. Methods A total of 181 male Sprague–Dawley SAH rats with the endovascular perforation model were utilized. Intraperitoneal MitoQ was given 1 h (h) post-SAH. Cerebroventricular ML385, an inhibitor of NF-E2-related factor 2 (Nrf2) and Small interfering ribonucleic acid (siRNA) for Prohibitin 2 (PHB2) were injected respectively 24 h and 48 h before SAH. Neurological function evaluation was performed before sacrifice. SAH grade was measured during the sacrifice of each animal. Brain water content was performed at 24 h. Co-immunoprecipitation was used to demonstrate the relationship of proteins Nrf2 and PHB2. Mitochondrial and cytoplasmic fractions were gathered using mitochondria isolation kits. Pathway related proteins were investigated with Western blot and immunofluorescence staining. Transmission electron microscopy was performed for mitochondrial morphology. Results Expression of Nrf2 levels peaked at the 3 h time point following SAH and then decreased to normal levels at 24 h, while PHB2 and Optic Atrophy 1 (OPA1) decreased at 24 h and 72 h after SAH compared with the Sham group. MitoQ treatment attenuated neurological deficits and brain edema, thereby resulting in a decreased expression of Albumin, while an increase of Nrf2, PHB2, OPA1 and Claudin-5 proteins compared with SAH + vehicle group. With co-immunoprecipitation, Nrf2 and PHB2 were further demonstrated to show their interaction. And MitoQ administration lead to more binding of the two proteins. ML385 abolished the effects of MitoQ on neurobehavior and protein levels post-SAH. Similarly, PHB2 siRNA reversed the neuroprotection of MitoQ administration with the decreased expression of PHB2 and OPA1 after SAH. Further, MitoQ treatment improved mitochondrial morphology after SAH with an increase of PHB2 and OPA1 in mitochondrial extraction. Conclusions MitoQ attenuates blood-brain barrier disruption via Nrf2/PHB2/OPA1 pathway after SAH in rats. MitoQ may serve as a potential therapeutic strategy for SAH patients.

Apelin, an endogenous ligand for the orphan G-protein-coupled receptor APJ, possesses anti-apoptotic and neuroprotective properties. It has been shown to be a protective factor for different types of central nervous system insults, such as ischemia and traumatic brain injury. Here, we investigated the effects of apelin-13 on early brain injury (EBI) following subarachnoid hemorrhage (SAH), and the underlying molecular mechanisms involved. Apelin-13 was delivered to rats via intracerebroventricular administration. Neurological scores, brain water content and neuronal apoptosis were measured 24 h after SAH. The PI3K/Akt inhibitor LY294002 or GLP-1R siRNA were injected into the lateral cerebral ventricle before induction of SAH. Changes in the expression of p-Akt, GLP-1R and apoptosis-associated proteins (Bax, Bcl-2, cleaved caspase-3) were then investigated. Results showed that the levels of GLP-1R in neurons increased significantly, reaching a peak at 24 h after the induction of SAH. Treatment with apelin-13 improved neurological deficits, as well as alleviated brain edema and apoptotic cell death. Apelin-13 was also able to increase the levels of p-Akt, GLP-1R and Bcl-2, while inhibiting the expression levels of Bax and cleaved caspase-3. The anti-apoptotic and neuroprotective effects of apelin-13 were partially reversed by addition of LY294002 or GLP-1R siRNA. These results provide evidence that apelin-13 attenuates EBI following SAH via suppressing neuronal apoptosis, and that this effect may act partially via the activation of the GLP-1R/PI3K/Akt signaling pathway.

Background and Purpose. T0901317, a liver X receptor (LXR) agonist, is widely used to explore the functions of LXRs. T0901317 exerts antiapoptotic effects in many central nervous system disease models. Our aim was to detect the role of T0901317 in neuronal apoptosis in early brain injury after subarachnoid hemorrhage. Methods. Subarachnoid hemorrhage (SAH) models of Sprague-Dawley rats were established with perforation method. T0901317 was injected intraperitoneally 1-hour post-SAH. GSK2033, an inhibitor of LXRs, and interferon regulatory factor (IRF-1) CRISPR activation were injected intracerebroventricularly to evaluate potential signaling pathway. The severity of SAH, neurobehavior test in both short- and long-term and apoptosis was measured with Western blot and immunofluorescence staining. Results. Expression of LXR-α and IRF-1 increased and peaked at 24 h post-SAH, while LXR-β remained unaffected in SAH+vehicle group compared with Sham group. Post-SAH T0901317 treatment attenuated neuronal impairments in both short- and long-term and decreased neuronal apoptosis, the expression of IRF-1, P53 upregulated modulator of apoptosis (PUMA), dynamin-1-like protein (Drp1), Bcl-2-associated X protein (Bax) and cleaved caspase-3, and increasing B-cell lymphoma 2 (Bcl-2) at 24 h from modeling. GSK2033 inhibited LXRs and reversed T0901317’s neuroprotective effects. IRF-1 CRISPR activation upregulated the expression of IRF-1 and abolished the treatment effects of T0901317. Conclusion. T0901317 attenuated neuronal apoptosis via LXRs/IRF-1/PUMA/Drp1 pathway in SAH rats.

Background and Objective. Whether anterior cerebral artery occlusion occurs after pipeline embolization devices (PEDs) are implanted to treat posterior communicating artery aneurysm is controversial. The purposes of this study were to explore the effect of a PED covering A1 on patients’ clinical prognosis and to evaluate the factors related to vascular occlusion. Method. The clinical and imaging data of PEDs in the postmarket multicenter registry study (PLUS) in China were retrospectively analyzed, and patients were divided into two groups on the basis of the follow-up angiographic results: group 1 (no significant change in A1 blood flow) and group 2 (A1 occlusion or decreased blood flow). We collected patients’ baseline data and evaluated the following imaging indicators: diameter and ratio of bilateral A1, M1, and internal carotid artery (ICA) vessels before stenting and the ratio of the PED size (sPED) to the ipsilateral ICA (I-ICA) diameter on the implantation side. Results. A total of 1171 patients were included, of whom 48 met the inclusion criteria (17 in group 1 and 31 in group 2). In group 2, three patients experienced neurological deterioration at follow-up. From the univariate analysis of outcomes, single PED without coils, incomplete aneurysm occlusion (IAO), maximum aneurysm diameter, aneurysms involving the ICA bifurcation (ICAb), and large sPED/I-ICA diameter ratio were included in the multivariate analysis ( P < 0.20 ). The multivariate regression analysis results showed that the ratio of sPED/I-ICA diameter was the factor influencing A1 vessel occlusion. The area under the ROC curve was 73.2%. When the sPED/I-ICA diameter ratio was 1.14, sensitivity was 70.6%, and specificity was 77.4%. Conclusion. When an oversized PED is placed from M1 to the ICA, the higher porosity formed at the covered A1 orifice is conducive to maintaining stable A1 blood flow and reducing the risk of A1 vessel occlusion. This trial is registered with ClinicalTrials.gov identifier: NCT03831672.

Background We have previously verified the beneficial effects of exosomes from endothelial progenitor cells (EPC-EXs) in ischemic stroke. However, the effects of EPC-EXs in hemorrhagic stroke have not been investigated. Additionally, miR-137 is reported to regulate ferroptosis and to be involved in the neuroprotection against ischemic stroke. Hence, the present work explored the effects of miR-137-overexpressing EPC-EXs on apoptosis, mitochondrial dysfunction, and ferroptosis in oxyhemoglobin (oxyHb)-injured SH-SY5Y cells. Methods The lentiviral miR-137 was transfected into EPCs and then the EPC-EXs were collected. RT-PCR was used to detect the miR-137 level in EPCs, EXs, and neurons. The uptake mechanisms of EPC-EXs in SH-SY5Y cells were explored by the co-incubation of Dynasore, Pitstop 2, Ly294002, and Genistein. After the transfection of different types of EPC-EXs, flow cytometry and expression of cytochrome c and cleaved caspase-3 were used to detect the apoptosis of oxyHb-injured neurons. Neuronal mitochondrial function was assessed by reactive oxygen species (ROS) level, mitochondrial membrane potential (MMP) depolarization, and cellular ATP content. Cell ferroptosis was measured by lipid peroxidation, iron overload, degradation of glutathione, and glutathione peroxidase 4. Additionally, recombinational PGE2 was used to detect if activation of COX2/PGE2 pathway could reverse the protection of miR-137 overexpression. Results The present work showed (1) EPC-EXs could be taken in by SH-SY5Y cells via caveolin-/clathrin-mediated pathways and macropinocytosis; (2) miR-137 was decreased in neurons after oxyHb treatment, and EXsmiR-137 could restore the miR-137 levels; (3) EXsmiR-137 worked better than EXs in reducing the number of apoptotic neurons and pro-apoptotic protein expression after oxyHb treatment; (4) EXsmiR-137 are more effective in improving the cellular MMP, ROS, and ATP level; (5) EXsmiR-137, but not EXs, protected oxyHb-treated SH-SY5Y cells against lipid peroxidation, iron overload, degradation of glutathione, and glutathione peroxidase 4; and (6) EXsmiR-137 suppressed the expression of the COX2/PGE2 pathway, and activation of the pathway could partially reverse the neuroprotective effects of EXsmiR-137. Conclusion miR-137 overexpression boosts the neuroprotective effects of EPC-EXs against apoptosis and mitochondrial dysfunction in oxyHb-treated SH-SY5Y cells. Furthermore, EXsmiR-137 rather than EXs can restore the decrease in miR-137 levels and inhibit ferroptosis, and the protection mechanism might involve the miR-137-COX2/PGE2 signaling pathway.

Background Intracranial artery atherosclerotic stenosis (ICAS) is among the causes of intracranial large artery occlusion (LVO). The optimal treatment strategy for patients with ischemic stroke due to ICAS-related LVO remains unclear. In this retrospective case series, we discussed our experience with direct angioplasty as frontline therapy for ICAS-related LVO. Methods We extracted data for patients who had a known pre-existing ICAS and undergone direct angioplasty as frontline therapy for ICAS-related LVO in the anterior circulation at our institution between January 2019 and December 2019. We analysed procedural details, the degree of reperfusion, functional outcomes, and complications. Successful reperfusion was defined as a modified Treatment in Cerebral Ischemia (mTICI) score of 2 b − 3. Functional outcomes at 90 days were assessed using modified Rankin Scale (mRS) scores (good outcome: mRS of 0–2). Results We analysed data for five patients (mean age: 51.6 ± 11 years). The mean time from symptom onset to recanalization was 371 ± 38.6 min. Occlusions involved the first segment of the middle cerebral artery in four patients and the intracranial internal carotid artery in one patient. Successful reperfusion was achieved in four (80%) patients. The remaining patient (20%) underwent intracranial stenting as rescue therapy, achieving a final mTICI of 2a. No re-occlusion was observed on follow-up images. Four patients (80%) achieved good outcomes at 90 days. There were no cases of symptomatic intracranial hemorrhage, although asymptomatic intracranial haemorrhage was observed in one patient. Conclusion Direct angioplasty may represent an alternative treatment strategy in patients with acute ischemic stroke due to known ICAS-related LVO.

IntroductionDelayed cerebral ischaemia (DCI) caused by aneurysmal subarachnoid haemorrhage (aSAH) is the most frequent complication and typically contributes to poor neurological outcome or deterioration of patients’ condition. Therefore, early accurate and effective prediction of DCI is urgently needed. This study aims to construct a dynamic nomogram for precisely calculating the risk of DCI in patients with aSAH. Internal validation of this tool is conducted using the training cohort, and independent external validation is completed by using other medical centre datasets.Methods and analysisThis study is a multicentre, retrospective, observational cohort study using data from patients with aSAH. The participants include all adult patients who received surgical treatment in neurosurgery of multiple medical centres from 1 September 2019 to 1 April 2021, including Renmin Hospital of Wuhan University, Huzhou Central Hospital, First Affiliated Hospital of Harbin Medical University, General Hospital of Northern Theatre Command and Affiliated Hospital of Panzhihua University. Clinical information is collected via the electronic medical record system, including demographic data, clinical state on admission and serum laboratory tests. Modified Fisher grade at admission, admission subarachnoid clot and cerebral oedema density, and residual postoperative subarachnoid clot density are determined using the electronic imagine record software. The primary outcome is DCI.Ethics and disseminationThis study protocol was reviewed and approved by the Medical Ethics Committee of Renmin Hospital of Wuhan University, which is the principal affiliation of this study (approval number: WDRM2021-K022). The other Ethics Committees, including Huzhou Central Hospital (approval number: 202108005–01), First Affiliated Hospital of Harbin Medical University (approval number: H202156), General Hospital of Northern Theater Command (approval number: Y2021060) and Affiliated Hospital of Panzhihua University (approval number: 202105002), also approved the protocol. The results of this research will be published in a peer-reviewed medical journal.Trial registration numberChiCTR2100044448.

The treatment of brain arteriovenous malformations (AVMs) remains a significant challenge, especially hemorrhagic AVMs which are unsuitable for microsurgery or radiosurgery. We demonstrate an AVM located in the left basal ganglia area, supplied by slender arteries, and treated by the transvenous pressure cooker technique. Herein, we describe the procedure and outline the crucial points and indications for this technique.

Background: Intracranial angioplasty and stenting is an optional treatment for patients with symptomatic intracranial artery stenosis (IAS) who have failed to respond to standard medical therapy. We aimed to analyze the effect of the operator’s learning curve in our center in terms of the safety of intracranial angioplasty and stenting. Methods: In this retrospective study, we analyzed patients treated with intracranial angioplasty and stenting in our center between January 2007 and December 2015. The endpoint was peri-procedure complications within 30 days. A risk-adjusted cumulative sum chart was used for the learning curve analysis. Multivariable logistic analysis was also used to evaluate the effect of the learning curve on intracranial angioplasty and stenting. Results: A total of 329 patients were included. The overall peri-procedure complication rate was 8.21% (27/329). Multivariate logistic regression analysis showed that operators with experience of >20 cases [odds ratio (OR) =0.229; 95% confidence interval (CI): 0.059–0.893] and >40 cases (OR =0.024; 95% CI: 0.006–0.093) were associated with a low risk of complications compared with operators with experience of ≤20 cases. Furthermore, patients with hypertension (OR =3.595; 95% CI: 1.104–11.702) and stenosis of Mori classification C (OR =28.562; 95% CI: 4.788–170.395) were associated with a high risk of complications. The observed outcome was better than expected (more negative deflections) after the 30th consecutive case. Conclusions: The level of operator experience can influence the risk of peri-procedure complications associated with intracranial angioplasty and stenting. A total of 30 consecutive cases is required for an operator to overcome the learning curve.

The purpose of this study was to evaluate the neuroprotective effects of astaxanthin on early brain injury (EBI) caused by subarachnoid hemorrhage (SAH) in rats and to explore possible molecular mechanisms. Experimental SAH model was introduced in adult male SD rats by injecting autologous arterial blood into the prechiasmatic cistern. Astaxanthin (75 mg/kg bodyweight) or olive oil was administered by oral gavage at 3 h after SAH. Our results showed that astaxanthin attenuated SAH-induced cerebral vasospasm and reduced neuronal apoptosis. Astaxanthin inhibited mitochondria-associated neuron apoptosis in the prefrontal cortex after SAH: increased mitochondrial membrane potential, decreased Bax/Bcl-2 ratio, inhibited cytochrome C release in cytoplasm, and suppressed caspase-3 enzyme activity. Furthermore, the cerebral expression levels of synaptic proteins (Synapsin-1, postsynaptic density-95 and growth-associated protein-43) and nerve growth and neuronal differentiation factors (brain-derived neurotropic factor and purine-rich binding protein-alpha) were reduced following SAH. Astaxanthin partly restored their expression. In conclusion, our current work demonstrates that astaxanthin attenuates SAH-induced EBI, possibly by improving neuronal survival and mitochondrial function.

Background: Ruptured tiny intracranial aneurysms (TIAs) have been challenging both for endovascular and neurosurgical interventions. Thus, we aimed to evaluate the safety and efficacy of low-profile visualized intraluminal support (LVIS) device in the treatment of ruptured TIAs (rTIAs). Material and Methods: Among 761 intracranial aneurysms which were treated either surgically or endovascularly, 32 rTIAs underwent stent-assisted coiling with LVIS device between 2014 and 2017. Patient data were reviewed retrospectively. Clinical and radiological outcomes were recorded at discharge and mid-term follow-up. Results: Mean patient ages were 53 ± 14.5 years. Mean aneurysm size was 2.28 ± .53 mm (range, 1-2.9 mm) with a mean dome:neck ratio of 1.08 (range, .75-2.14). The LVIS stents were successfully implanted in all patients. Mean follow-up period was 9.3 ± 1.9 months (range, 6-15 months). Immediate angiographic evaluation demonstrated complete occlusion in 13 (40.6%) patients, while neck remnant and residual sac were observed in 12 (37.5%) and 7 (21.9%), respectively. All patients had moderate disability (mRS 2-3) at discharge. Number of aneurysms with complete occlusion significantly increased and 82.1% of the patients (23 of 28) demonstrated complete occlusion at follow-up (P = .0015). Among these, 27 had good outcome (mRS 0-1; 96.9%) with significant improvement compared to discharge (P = .0001). There was no recurrence or enlargement of the residual aneurysms. Additionally, there were no procedure-related complications except the one (3.6%) showing asymptomatic stenosis of the posterior cerebral artery in follow-up imagings. Conclusions: Stent-assisted coiling of rTIAs with LVIS device provides high rates of technical success and complete occlusion at mid-term follow-up with an excellent safety profile.

Mitochondrial dysfunction is considered a crucial therapeutic target for early brain injury following subarachnoid hemorrhage (SAH). Emerging evidence indicates that docosahexaenoic acid (DHA), an essential omega-3 fatty acid, protects mitochondria in various chronic diseases. This study aimed to investigate the neuroprotective effects of DHA on mitochondrial dynamic dysfunction after EBI using in vivo and in vitro approaches. For in vivo experiments, the rat endovascular perforation SAH model was performed, whereby DHA was administered intravenously 1 h after induction of SAH. Primary cultured neurons treated with oxyhemoglobin (OxyHb) for 24 h were used to mimic SAH in vitro. Our results demonstrated that DHA improved neurological deficits and reduced brain edema in rats with SAH, and attenuated OxyHb-induced neuronal death in primary cultured cells. DHA reduced the amount of reactive oxygen species-positive cells and improved cell viability when compared to the SAH + vehicle group in vitro. DHA attenuated malondialdehyde levels and superoxide dismutase stress, increased Bcl2 and Bcl-xl, and decreased Bax and cleaved caspase-3 in vivo. Additionally, DHA ameliorated mitochondrial dysfunction, upregulated the mitochondrial fusion-related protein Optic Atrophy 1, and downregulated the mitochondrial fission-related protein Dynamin-Related-Protein 1 (Drp1) and Serine 616 phosphorylated Drp1 after SAH both in vitro and in vivo. Taken together, our current study demonstrates that DHA might prevent oxidative stress-based apoptosis after SAH. The characterization of the underlying molecular mechanisms may further improve mitochondrial dynamics-related signaling pathways.

Hemorrhagic stroke is associated with high morbidity and mortality. Hemin is a decomposition product of hemoglobin that is related to neuronal apoptosis after hemorrhage, although the molecular basis for this association remains unclear. To address this issue, the present study investigated hemin-induced changes in the apoptotic index and mitochondrial ultrastructure in SH-SY5Y cells. Cell viability was evaluated using Cell Counting Kit-8 and by terminal transferase dUTP nick-end labeling, western blotting, and flow cytometry. Changes in mitochondrial ultrastructure were examined by super-resolution three-dimensional structured illumination microscopy. We found that cleaved-caspase-3 expression and the number of apoptotic cells increased in a time-dependent manner upon hemin treatment, which was associated with mitochondrial fragmentation. Our data suggest that hemin induces apoptosis and mitochondrial fission in neuronal cells. Thus, therapeutic strategies that target hemin could mitigate the damage caused by hemorrhagic stroke.

Hyperperfusion syndrome (HPS) is a rare but potentially devastating postoperative complication developing after endarterectomy and carotid stenting. Limited information is available about this complication. The aim of this study was to assess the incidence of HPS and risk factors leading to its development. We retrospectively reviewed 178 consecutive cases of patients who underwent stenting of intracranial artery revascularization. We analyzed the association between HPS and patient’s age, collateral vascular supply of the lesion, the interval between operation and the last occurrence of ischemic symptom, adequacy of blood pressure control after the operation, and other risk factors such as diabetes, smoking, hypertension, and gender. Of 178 included patients, we found HPS in six cases (3.4 %). Failure to strictly control postoperative blood pressure, a less than 3-week long interval between operation and the last occurrence of ischemic symptom, and poor collateral circulation were significantly associated with the development of HPS. The aforementioned factors are predictors for HPS. We argue that nitroprusside should not be used to control blood pressure after the operation because its use permits considerable blood pressure fluctuations.

A recent genome-wide association study has identified an association between rs1920116 near TERC and high-grade glioma in populations of European ancestry. In order to evaluate the effect of the SNP rs1920116 near TERC in the Chinese population, we examined associations of this candidate SNP with glioma in a sample of 1970 Chinese Han individuals. SNP genotype data were available for 980 Chinese glioma patients and 990 healthy controls. Logistic regression analyses were performed to evaluate the association between rs1920116 and glioma risk adjusted for age, gender and stratified by tumor grade where appropriate. The allele G at TERC rs1920116 are risk factors for gliomas, and its association with glioma risk was consistent across tumor subgroups in the Chinese Han population (OR = 1.18–1.21). In order to assess variation in SNP effect size at different patient ages, glioma cases and controls were divided into 3 age strata, in years

Subarachnoid hemorrhage (SAH) is an important cause of mortality in stroke patients. Long non-coding RNAs (LncRNAs) have important functions in brain disease, however their expression profiles in SAH remain to be elucidated. The present study aimed to investigate the expression signatures of LncRNAs and mRNAs in early brain injury (EBI) following SAH in a rat model. Male Wistar rats were randomly divided into an SAH group and a sham operation group. The expression signatures of the LncRNAs and mRNAs in the temporal lobe cortex were investigated using a rat LncRNAs array following experimental SAH. The results revealed that there were 144 downregulated and 64 upregulated LncRNAs and 181 downregulated and 221 upregulated mRNAs following SAH. Additionally, two upregulated (BC092207, MRuc008hvl) and three downregulated (XR_006756, MRAK038897, MRAK017168) LncRNAs were confirmed using reverse transcription quantitative polymerase chain reaction. The differentially expressed mRNAs were further analyzed using the Gene Ontology and the Kyoto Encyclopedia of Genes and Genomes (KEGG) databases. The pathway analysis results provided by the KEGG database indicated that eight pathways associated with inflammation were involved in EBI following SAH. In conclusion, these results demonstrated that the expression profiles of the LncRNAs and mRNAs were significantly different between the SAH-induced EBI group and the sham operation group. These differently expressed LncRNAs may be important in EBI following SAH.

We report a case of 57-year-old man with bilateral thalamic infarction due to a DAVF, who underwent a mistreatment initially. We found simple medication was ineffective in treatment of bilateral thalamic infarct due to DVAF, and patients might have a better outcome if surgery was performed in prophase of disease. Further more, MRA and DSA should be as a routine examination for patients suspected with venous infarction for differences therapies.

The objective of the present study was to evaluate the correlation between sympathetic nerve activation and inflammatory response in the acute stage of subarachnoid hemorrhage (SAH) in a canine perforating model. SAH was induced by perforation of the basilar artery with the use of a microcatheter via the femoral artery in 20 mongrel dogs. Hemodynamic parameters and intracranial pressure were recorded, and blood sample for C3a, C5b-9, IL-6, IL-8 and noradrenaline kinetic determination were measured at 0, 5, 15, 30, 60, 120, and 180 min after SAH. Noradrenaline (pg/mL) increased abruptly from 104+/-59 to 2010+/-918 at 5 min after SAH. C3a and C5b-9 reached peak values at 15 min and IL-6 and IL-8 reached peak values at 30 min after SAH, respectively. The peak values of C3a and C5b-9 correlated positively with the peak value of noradrenaline (r=0.743 and r=0.753, respectively). The peak values of IL-6 and IL-8 also correlated positively with the peak values of noradrenaline (r=0.603 and r=0.681, respectively).These results suggest that a pronounced activation of the sympathetic nervous system and the inflammatory response occurs in acute stage of SAH. Significant association between the rate of spillover of norepinephrine to plasma and the plasma levels of inflammatory markers indicates that the two processes, sympathetic activation and immune response are quantitatively linked in early stage after SAH. The exact mechanisms underlying this phenomenon deserved further investigations.