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We aimed to describe the initial experience of mechanical thrombectomy using tandem double stent retrievers combined with intermediate catheter aspiration to treat refractory severe hemorrhagic (SH)-cerebral venous sinus thrombosis (CVST). All refractory SH-CVST patients treated with mechanical thrombectomy using tandem double stent retriever (SR) combined with intermediate catheter aspiration (MT-TDSA) in our institution were retrospectively reviewed. MT-TDSA is a technique that fully engages the clot with double SRs and retrieves the clot using a double SR in combination with aspiration from an intermediate catheter. Demographics, clinical manifestation, medical history, the location of the occluded venous sinus, intraoperative details, procedure-related complications, and modified Rankin Scale (1, 6, 12 months postoperatively) were collected and analyzed. Fourteen patients (median age, 43 years) with refractory SH-CVST were treated with MT-TDSA between January 2016 and January 2020. Ten of 14 (71.4%) had a successful intraoperative recanalization rate (>90%) using MT-TDSA. No procedure-related complications occurred. Eleven patients had good clinical outcomes (modified Rankin Scale score 0–2 at 12 months postoperatively). MT-TDSA for refractory SH-CVST might improve clot-capturing ability and remove blood clots from cerebral venous sinuses effectively and safely, achieving good clinical outcomes. [ABSTRACT FROM AUTHOR]

Objective Glioblastoma (GBM), a type of malignant glioma, is the most aggressive type of brain tumor and is associated with high mortality. Hexose-6-phosphate dehydrogenase (H6PD) has been detected in multiple tumors and is involved in tumor initiation and progression. However, the specific role and mechanism of H6PD in GBM remain unclear. Methods We performed pan-cancer analysis of expression and prognosis of H6PD in GBM using the Genotype-Tissue Expression Project (GTEx) and The Cancer Genome Atlas (TCGA). Subsequently, noncoding RNAs regulating H6PD expression were obtained by comprehensive analysis, including gene expression, prognosis, correlation, and immune infiltration. Finally, tumor immune infiltrates related to H6PD and survival were performed. Results Higher expression of H6PD was statistically significantly associated with an unfavorable outcome in GBM. Downregulation of hsa-miR-124-3p and hsa-miR-516b-5p in GBM was detected from GSE90603. Subsequently, OSMR-AS1 was observed in the regulation of H6PD via hsa-miR-516b-5p. Moreover, higher H6PD expression significantly correlated with immune infiltration of dendritic cells, immune checkpoint expression, and biomarkers of dendritic cells. Conclusions The OSMR-AS1/ miR-516b-5p axis was identified as the highest-potential upstream ncRNA-related pathway of H6PD in GBM. Furthermore, the present findings demonstrated that H6PD blockading might possess antitumor roles via regulating dendritic cell infiltration and immune checkpoint expression. [ABSTRACT FROM AUTHOR]

• The inverse variance weighted method was used in this MR study. • Genetically predicted epilepsy did not causally increase the risk of memory loss. • Confounding or nongenetic determinants may influenced previous associations. Epidemiological studies have reported an association between epilepsy and dementia. However, the causal relationship between epilepsy and the risk of dementia is not clear. We aimed to inspect the causal effect of epilepsy on memory loss and dementia. We analyzed summary data of epilepsy, memory loss, and dementia from the genome-wide association study (GWAS) using the two-sample Mendelian randomization (MR) method. We used the estimated odds ratio of memory loss and dementia associated with each of the genetically defined traits to infer evidence for a causal relationship with the following exposures: all epilepsy, focal epilepsy (including focal epilepsy with hippocampal sclerosis, lesion-negative focal epilepsy, and focal epilepsy with other lesions), and genetic generalized epilepsy (including childhood absence epilepsy, generalized tonic-clonic seizures alone, Juvenile absence epilepsy, and Juvenile myoclonic epilepsy). According to the result of MR using the inverse variance weighted method (IVW), we found that genetically predicted epilepsy did not causally increase the risk of memory loss and dementia (p > 0.05). Results of the MR-Egger and weighted median method were consistent with the IVW method. No evidence has been found to support the notion that epilepsy can result in memory loss and dementia. The associations observed in epidemiological studies could be attributed, in part, to confounding or nongenetic determinants. [ABSTRACT FROM AUTHOR]

Background and Objective: The aim of the study is to investigate the value of serum iron and hemoglobin levels for predicting acute seizures following aneurysmal subarachnoid hemorrhage (aSAH).Methods: Clinical and laboratorial data from patients with ruptured intracranial aneurysms were collected in the retrospective study. Age, sex, symptom onset, history of diabetes and hypertension, history of coronary artery disease, temperature, Hunt-Hess grade, Fisher grade, aneurysm location, hemoglobin, serum potassium, sodium, calcium, phosphorus, and iron were collected. Acute seizures were determined as seizures within 1 week following aSAH. Propensity score matching (PSM) analyses were performed to correct imbalances in patient characteristics between seizure and non-seizure groups.Results: A total of 760 patients were included. Incidence of acute seizures following aSAH was 6.4%. In the univariate analysis, significant differences were detected in age, admission Hunt-Hess grade, Fisher grade, hemoglobin, serum sodium, and serum iron between seizure and non-seizure groups. In multivariate logistic regression model, lower serum iron was considered as a risk factor for acute seizures (OR 0.182, 95% CI 0.084-0.393, p = 0.000), as well as lower hemoglobin (OR 0.977, 95% CI 0.962-0.993, p = 0.004) and higher serum sodium (OR 1.072, 95% CI 1.003-1.145, p = 0.039). After PSM, there were no significant differences in age, admission Hunt-Hess grade, Fisher grade, and serum sodium between seizure and non-seizure groups. The matched seizure group had lower serum iron and hemoglobin levels compared with the matched non-seizure group (p < 0.05). The optimal cutoff value for serum iron and hemoglobin levels as a predictor of acute seizure after aSAH was determined as 9.9 mmol/L (sensitivity was 81.63% and the specificity was 65.40%) and 119 g/L (sensitivity was 63.27% and the specificity was 70.18%), respectively.Conclusions: Serum iron and hemoglobin levels were inversely associated with a high risk of acute seizures following aSAH. [ABSTRACT FROM AUTHOR]

We tested the hypothesis that low serum iron levels are associated with acute hydrocephalus following aneurysmal subarachnoid hemorrhage (aSAH). Patients presenting with ruptured intracranial aneurysms were enrolled in the prospective observational study. Age, sex, history of diabetes, hypertension and hyperlipidemia, symptom onset, Fisher grade, Hunt-Hess grade, aneurysm location, hemoglobin, and serum iron were collected. Acute hydrocephalus was determined within 72 hours after subarachnoid hemorrhage. A propensity-score matching analysis was performed to correct imbalances in patient characteristics between hydrocephalus and non-hydrocephalus groups. A total of 535 patients were included. Incidence of acute hydrocephalus was 20.0%. In multivariate logistic regression analysis, lower serum iron was considered as a risk factor of acute hydrocephalus, as well as delayed ischemic neurologic deficit and lower hemoglobin (P = 0.000). After propensity-score matching, lower serum iron was considered as an independent risk factor for acute hydrocephalus, whereas hemoglobin and delayed ischemic neurologic deficit were not. The matched hydrocephalus group had lower serum iron comparing with the matched non-hydrocephalus group (10.26 ± 5.33 mmol/L vs. 13.44 ± 5.18 mmol/L; P = 0.000). The optimal cut-off value for serum iron levels as a predictor for acute hydrocephalus in patients with aSAH was determined as 13.1 mmol/L in the receiver operating characteristic curve. Furthermore, lower serum iron levels (odds ratio 0.305; 95% confidence interval, 0.178–0.524; P = 0.000) and acute hydrocephalus (odds ratio 0.372; 95% confidence interval, 0.202–0.684; P = 0.001) were predictors of poor outcome, as well as higher Hunt-Hess grade and Fisher grade. Lower serum iron levels after aSAH was a predictor of acute hydrocephalus and unfavorable outcome. [ABSTRACT FROM AUTHOR]

Objective We tested the hypothesis that cerebellopontine angle (CPA) tumors are associated with a greater incidence of unruptured intracranial aneurysms (IAs). Methods Patients with intracranial tumors (ITs) undergoing computed tomography angiography and magnetic resonance imaging were enrolled in an observational cohort study that prospectively collected age, sex, hypertension, diabetes, cerebral arteriosclerosis, tumor type, tumor location, hydrocephalus, smoking, alcohol intake, CPA tumor size, cerebral aneurysms, and cerebral arteriosclerosis. Patients with the coexistence of IA and IT were classified as group II, whereas the others with IT as group I. Results We included 1218 patients with IT for analysis. The incidence of IA was 7.1% (86/1218). A total of 31% of patients with aneurysms had CPA tumors. In a multivariate logistic regression model, a greater incidence of IA was found in female patients (odds ratio [OR] 1.726, 95% confidence interval [CI] 1.050–2.836, P = 0.031) and in patients with CPA tumors (OR 3.002, 95% CI 1.822–4.947, P = 0.000) after adjustment for tumor type, cerebral arteriosclerosis, and age. In female patients, CPA tumors were a unique independent risk factor of a greater incidence of IA (OR 2.270, 95% CI 1.194–4.317, P = 0.012). Furthermore, cerebral arteriosclerosis was a unique independent risk factor of IA in patients with CPA tumors (OR 7.626, 95% CI 2.928–19.860, P = 0.000). Conclusions These data support the hypothesis that CPA tumors are associated with a greater incidence of unruptured IAs, especially in female patients. Cerebral arteriosclerosis contributed to elevated risk of IA in patients with CPA tumors. [ABSTRACT FROM AUTHOR]

Background and Objective We tested the hypothesis that ionized calcium levels at admission are associated with early hematoma expansion and functional outcome in patients with hypertensive intracerebral hemorrhage (HICH). Methods Patients presenting with HICH were enrolled in the observational cohort study that prospectively collected age, sex, blood pressure, history of diabetes and smoking, time from symptom onset to initial computed tomography (CT), admission ionized calcium (iCa) and total calcium (tCa), coagulation function, Glasgow Coma Scale (GCS), and postoperative modified Rankin Scale score. Hematoma reconstruction on CT was performed to measure hematoma volumes. Hematoma expansion (HE) was defined as an increase of more than 30% or 6 mL in HICH volume. We performed univariate and multivariate analyses to assess for association of iCa level with early HE and functional outcome. Results We included 111 patients with HICH for analysis. Admission serum iCa was 1.10 mmol/L in patients with HE and 1.17 in patients without HE. Univariate analysis indicated significant difference of GCS, initial HICH volume, iCa, and tCa between the HE and non-HE groups (P < 0.05). Lower admission iCa (less than 1.12 mmol/L) was associated with HE (odds ratio [OR] 0.300, 95% confidence interval [CI] 0.095–0.951, P = 0.041) after adjustment for age, blood pressure, GCS score, time to initial CT scan, baseline HICH volume, prothrombin time, and tCa. Furthermore, predictive factors of poor outcome included iCa (OR 0.192, 95% CI 0.067–0.554, P = 0.002) and GCS score (OR 0.832, 95% CI 0.722–0.959, P = 0.011). Conclusions These data support the hypothesis that lower ionized calcium is associated with early hematoma expansion and poor outcome in patients with hypertensive intracerebral hemorrhage. Highlights • Lower iCa levels were associated with a greater risk of hematoma expansion. • A lower iCa level was an independent risk factor for a poor outcome at 3 months. • Serum iCa level was inversely correlated with systolic blood pressure. • Serum tCa and iCa on admission predicted greater baseline HICH volume. • Serum iCa accurately reflects the physiologically active component in HICH. [ABSTRACT FROM AUTHOR]

To identify susceptible biomarkers for the development of bipolar disorder (BD), we conducted a Mendelian Randomization (MR) design to screen circulating proteins for the potential risk of bipolar disorder systematically. We performed a two-sample Mendelian randomization (MR) analysis to estimate the causality of 4782 human circulating proteins on the risk of bipolar disorder. 376 circulating biomarkers were selected in MR estimation (4406 circulating proteins with less than 3 SNPs were excluded) with 5368 European descents. GWAS meta-analysis of the potential role of all-cause bipolar disorder arose from the Psychiatric Genomics Consortium (41,917 cases, 371,549 controls). After IVW and sensitivity analysis, 4 circulating proteins having causal effects on bipolar disorder were identified. ISG15, as a key player in the innate immune response, decreased the risk of bipolar disorder causally (OR = 0.92, 95% CI = 0.89–0.94, P = 1.46e-09). Furthermore, MLN decreased the risk of bipolar disorder causally (OR = 0.94, 95% CI = 0.91–0.97, P = 1.04e-04). In addition, SFTPC (OR = 0.91, 95% CI = 0.86–0.96, P = 4.47e-04) and VCY (OR = 0.86, 95% CI = 0.77–0.96, P = 8.55e-03) presented a suggestive association with bipolar disorder. Our findings indicated that ISG15 and MLN showed evidence of causality in bipolar disorder and provided a promising target for the diagnosis and treatment of diseases. [ABSTRACT FROM AUTHOR]

Treatment of blood blister-like aneurysms (BBAs) of the supraclinoid internal carotid artery (ICA) with flow diverters (FDs) has become widespread in recent years. However, ruptured blood blister-like aneurysm (BBA) of ICA treatment with flow diverter-assisted coil embolization (FDAC) remains controversial. Moreover, limited direct comparative studies have been conducted between the two treatment modalities, FDs and FDAC, for BBAs. The purpose of this study was to document our experience and evaluate the effectiveness and safety of FDAC. We conducted a retrospective analysis of clinical and radiological information from ten patients who experienced ruptured BBAs of the supraclinoid ICA at our center from January 2021 to February 2023. The technical details of FDAC for ruptured BBAs were described, and the technical steps were named "pipeline embolization device (PED)-Individualized shaping(microcatheter)-Semi deploying-Rivet(coils)-Massage(microwire)" as the PEISSERM technique. Clinical outcomes were assessed using the modified Rankin Scale (mRS), whereas radiological results were determined through angiography. A pooled analysis was implemented, incorporating data from literature sources that reported perioperative and long-term clinical and angiographic outcomes of ruptured BBAs treated with FD and FDAC strategies, along with our data. Data in our analysis pool were categorized into FD and FDAC strategy groups to explore the preferred treatment modalities for BBAs. The PEISSERM technique was utilized to treat ten patients, seven males, and three females, with an average age of 41.7 years. A single PED was deployed in conjunction with coils in all ten patients. All PEDs were documented to have good wall apposition. The immediate postoperative angiograms demonstrated Raymond grade I in ten aneurysms. Angiographic follow-up of nine patients at 4–25 months showed total occlusion of the aneurysms. At the most recent follow-up, the mRS scores of nine patients hinted at a good prognosis. Pooled analysis of 233 ICA-BBA cases of FD revealed a technical success rate of 91% [95% confidence interval (CI), 0.88 to 0.95], a rate of complete occlusion of 79% (95% CI, 0.73 to 0.84), a recurrence rate of 2% (95% CI, 0.00 to 0.04), a rebleed rate of 2% (95% CI, 0.00 to 0.04), and the perioperative stroke rate was 8% (95% CI, 0.04 to 0.11). The perioperative mortality was 4% (95% CI, 0.01 to 0.07). The long-term good clinical outcome rate was 85% (95% CI, 0.80 to 0.90). The mortality rate was 6% (95% CI, 0.03 to 0.09). Results from the subgroup analysis illustrated that the FDAC strategy for BBAs had a significantly higher immediate postoperative complete occlusion rate (P < 0.001), total occlusion rate (P = 0.016), and a good outcome rate (P = 0.041) compared with the FD strategy. The FDAC strategy can yield a higher rate of good outcomes than the FD strategy. The PEISSERM technique employed by the FDAC is a reliable and effective treatment approach as it can minimize the hemodynamic burden of BBA's fragile dome, thereby achieving an excellent occlusion rate. The PEISSERM technique in the FDAC strategy contributes to understanding the BBA's treatment and offers a potentially optimal treatment for BBA. [ABSTRACT FROM AUTHOR]

The majority of low-grade gliomas (LGGs) in adults invariably progress to glioblastoma over time. Spectrin β non-erythrocytic 2 (SPTBN2) is detected in numerous tumors and is involved in tumor occurrence and metastasis. However, the specific roles and detailed mechanisms of SPTBN2 in LGG are largely unknown. The present study performed pan-cancer analysis for the expression and prognosis of SPTBN2 in LGG using The Cancer Genome Atlas and The Genotype-Tissue Expression. Western blotting was used to detect the amount of SPTBN2 between glioma tissues and normal brain tissues. Subsequently, based on expression, prognosis, correlation and immune infiltration, non-coding RNAs (ncRNAs) were identified that regulated SPTBN2 expression. Finally, tumor immune infiltrates associated with SPTBN2 and prognosis were performed. Lower expression of SPTBN2 was correlated with an unfavorable outcome in LGG. A significant correlation between the low SPTBN2 mRNA expression and poor clinicopathological features was observed, including wild-type isocitrate dehydrogenase status (P<0.001), 1p/19q non-codeletion (P<0.001) and elders (P=0.019). The western blotting results revealed that, compared with normal brain tissues, the amount of SPTBN2 was significantly lower in LGG tissues (P=0.0266). Higher expression of five microRNAs (miRs/miRNAs), including hsa-miR-15a-5p, hsa-miR-15b-5p, hsa-miR-16-5p, hsa-miR-34c-5p and hsa-miR-424-5p, correlated with poor prognosis by targeting SPTBN2 in LGG. Subsequently, four long ncRNAs (lncRNAs) [ARMCX5-GPRASP2, BASP1-antisense RNA 1 (AS1), EPB41L4A-AS1 and LINC00641] were observed in the regulation of SPTBN2 via five miRNAs. Moreover, the expression of SPTBN2 was significantly correlated with tumor immune infiltration, immune checkpoint expression and biomarkers of immune cells. In conclusion, SPTBN2 was lowly expressed and correlated with an unfavorable prognosis in LGG. A total of six miRNAs and four lncRNAs were identified as being able to modulate SPTBN2 in a lncRNA-miRNA-mRNA network of LGG. Furthermore, the current findings also indicated that SPTBN2 possessed anti-tumor roles by regulating tumor immune infiltration and immune checkpoint expression. [ABSTRACT FROM AUTHOR]

Objective Cerebral ischemia is a major contributor to poor outcome after ruptured anterior communicating artery aneurysms (ACoAs), and is not well classified. In this article, we develop a classification and identify risk factors of cerebral ischemia after ruptured ACoAs. Methods Three hundred sixty patients with ruptured ACoAs undergoing microsurgical clipping were collected. Sex, age, smoking status, Hunt-Hess grade, Fisher grade, hospital stay, surgical timing, hypertension, diabetes, postoperative cerebral ischemia, and postoperative modified Rankin Scale score were collected. Postoperative ischemic changes are classified according to a novel grade (ischemic grade I–IV). Results Predictive factors of postoperative ischemia (grade I–IV) included sex (odds ratio [OR], 1.956; 95% confidence interval [CI], 1.262–3.032; P = 0.003) and Fisher grade (OR, 1.813; 95% CI, 1.144–2.871; P = 0.011). Male sex had a tendency to develop postoperative cerebral ischemia (61.3% in the ischemia group vs. 45.7% in the nonischemia group), while surgical timing did not. However, in patients with postoperative ischemia, early surgery within 3 days (OR, 3.334; 95% CI, 1.411–7.879; P = 0.006) and advanced age greater than 55 years (OR, 2.783; 95% CI, 1.214–6.382; P = 0.016) were risk factors for postoperative neurologic deficits (grade III–IV). Conclusions Male sex and higher Fisher grade predict postoperative ischemia (grade I–IV), whereas surgical timing does not. However, in patients with postoperative cerebral ischemia, early surgery within 3 days and age greater than 55 years can increase the frequency of postoperative neurological deficits (grade III–IV). Older male patients undergoing early microsurgery had a tendency to develop neurologic deficits. [ABSTRACT FROM AUTHOR]

This study aimed to investigate the association between serum iron (SI) and postoperative delayed cerebral ischemia (DCI) following aneurysmal subarachnoid hemorrhage (aSAH). We retrospectively analyzed 985 consecutive adult patients diagnosed with aSAH. Demographic, clinical, and laboratory data were recorded. Univariate and multivariate analyses were employed to assess the association between SI and DCI. Propensity-score matching (PSM) analysis was implemented to reduce confounding. Postoperative DCI developed in 14.38% of patients. Lower SI upon admission was detected in aSAH patients with severe clinical conditions and severe aSAH. SI was negatively correlated with WFNS grade (r = −0.3744, p < 0.001) and modified Fisher (mFisher) grade (r = −0.2520, p < 0.001). Multivariable analysis revealed lower SI was independently associated with DCI [odds ratios (OR) 0.281, 95% confidence interval (CI) 0.177–0.448, p < 0.001], while WFNS grade and mFisher grade were not. The receiver-operating characteristics (ROC) curve analysis of SI for DCI gave an area under the curve (AUC) of 0.7 and an optimal cut-off of 7.5 μmol/L (95% CI 0.665 to 0.733, p < 0.0001). PSM demonstrated the DCI group had a significantly lower SI than the non-DCI group (10.91 ± 6.86 vs. 20.34 ± 8.01 μmol/L, p < 0.001). Lower SI remained a significant independent predictor for DCI and an independent poor prognostic factor of aSAH in multivariate analysis (OR 0.363, 95% CI 0.209–0.630, p < 0.001). The predictive performance of SI for poor outcome had a corresponding AUC of 0.718 after PSM. Lower SI upon admission is significantly associated with WFNS grade, mFisher grade, and predicts postoperative DCI and poor outcome at 90 days following aSAH. [ABSTRACT FROM AUTHOR]

Brain retraction is required during many intracranial procedures to provide more working space. However, it is difficult to avoid brain retraction injury. Here, we report on retractorless surgery for anterior circulation aneurysms via a pterional keyhole approach. All patients undergoing a minimally invasive pterional keyhole approach within 3 days after hemorrhage by the same surgeon were included in the study. Patients were randomly assigned into group I (with the retractorless technique) and group II (with fixed retractors). Data on adequate clipping level, intraoperative ischemia induced by retraction, operation time, brain retraction injury, intraoperative blood loss, intraoperative aneurysm rupture, and modified Rankin Scale were collected for the 2 groups. A consecutive series of 47 patients (21 patients in group I, 26 patients in group II) successfully underwent a minimally invasive pterional keyhole approach. Statistical analysis revealed no significant between-group differences with regard to sex, age, Hunt-Hess grade, adequate clipping level, operation time, intraoperative blood loss, and aneurysm rupture ( P > 0.05). However, no intraoperative ischemia was detected in group I, whereas 23.1% (6 of 26) of patients in group II had reversible ischemia. Furthermore, the proportion of brain retraction injuries in group I (5.3%) was lower than that in group II (34.6%). In addition, a better prognosis was obtained in patients who underwent retractorless surgery. With the careful and accurate use of a handheld suction device and operating instruments, the retractorless technique can replace fixed retraction, reduce brain retraction injury, and is applicable to surgeries on anterior circulation aneurysms via pterional keyhole approaches. [ABSTRACT FROM AUTHOR]

The correct sentence should be: The matched DCI group had a significantly lower SI level than the matched non-DCI group (9.00 ± 6.29 vs. 20.13 ± 8.45 mol/L, I p i < 0.001) (Table 1 and Figure 2D). Admission Serum Iron as an Independent Risk Factor for Postoperative Delayed Cerebral Ischemia Following Aneurysmal Subarachnoid Hemorrhage: A Propensity-Matched Analysis. In Table 1, the number of patients from admission to surgical treatment (<=72 h) in the Non-DCI group was 77 after PSM. [Extracted from the article]

Purpose: The importance of supplementary motor area (SMA) for motor function and compensation for primary motor area (M1) has received increased attention. Methods: We used diffusion tensor imaging (DTI) and transcranial magnetic stimulation (TMS) to evaluate structure and function of corticospinal projection originating from SMA. Fibers of corticospinal projection originating from M1 (CST) and SMA (ACST) were analyzed. ACST originating from mesial SMA area formed separate white matter bundles leaving the anterior part of M1 area, which then entered the posterior limb of the internal capsule. Projection and overlap of both CST and ACST were detected on medulla. Results: Fibers of contralesional ACST were more than that of ipsilesional ACST in patients with SMA tumors (p<0.05). In patients with SMA tumor, all patients experienced temporary akinesia postoperatively. Seven hundred forty-one fibers of ipsilateral ACST and no fibers of ipsilateral CST were detected in the patient with M1 glioma, while most of contralateral limb movement was preserved. MEP could be evoked by stimulating SMA area as well as M1 area. ACST originated from SMA area and projected to the medial medulla. Conclusion: SMA area and ACST integrity contributed to contralateral motor function and were a compensation for M1 lesion and damaged CST. [ABSTRACT FROM AUTHOR]

This document is a correction notice for an article titled "Treatment with a flow diverter-assisted coil embolization for ruptured blood blister-like aneurysms of the internal carotid artery: a technical note and analysis of single-center experience with pooled data." The correction addresses an error in the affiliations of Dr. Kang, which have been corrected in this erratum article. The original article has been updated to reflect this correction. The publisher, Springer Nature, remains neutral regarding jurisdictional claims and institutional affiliations. [Extracted from the article]

We tested the hypothesis that low hemoglobin levels are associated with acute seizures after aneurysmal subarachnoid hemorrhage (aSAH). Patients with ruptured intracranial aneurysms were enrolled in the observational cohort study that prospectively collected age, sex, symptom onset, history of diabetes and hypertension, history of coronary artery disease, temperature, Hunt-Hess grade, Fisher grade, aneurysm location, hemoglobin, hematocrit, serum potassium, sodium, calcium, phosphorus, iron, and modified Rankin Scale. Acute seizures were determined as seizures within 1 week after aSAH. We included 554 patients with requisite data for analysis in the prospective study. Incidence of acute seizures following aSAH was 3.61%. In the univariate analysis, significant differences were detected in admission Hunt-Hess grade, Fisher grade, hemoglobin, and serum iron between epilepsy and nonepilepsy groups. Furthermore, acute seizures were associated with higher modified Rankin Scale score and poor outcome (P = 0.004). Serum hemoglobin levels were 114.30 ± 20.08 g/L in the epilepsy group, which were lower than those in the nonepilepsy group (128.64 ± 17.94 mmol/L, P = 0.001). Serum iron levels were 8.89 ± 5.03 g/L in the epilepsy group, which were also lower than those in the nonepilepsy group (13.71 ± 6.70 mmol/L, P = 0.002). The hemoglobin level was positively correlated with serum iron on admission (ρ = 0.321, P = 0.000). In the multivariate logistic regression model, lower hemoglobin was considered as an independent risk factor of acute seizures (odds ratio 4.286, 95% confidence interval 1.492–12.315, P = 0.007). The optimal cutoff value for hemoglobin level as a predictor for acute epilepsy after aSAH was determined as 119 g/L in the receiver operating characteristic curve (sensitivity was 75.00%, and specificity was 69.48%). These data support the hypothesis that hemoglobin was inversely associated with acute seizures following aSAH. [ABSTRACT FROM AUTHOR]

Objective To determine whether extended lesionectomy is needed for patients with cerebral cavernous malformations presenting with epilepsy as compared with lesionectomy. Methods A literature search of PubMed, Embase, Web of Science, Clinical Trials and Cochrane Central Register of Controlled Trials was performed for pertinent English-language studies from 1967 to 2017. Eligible studies were selected according to uniform inclusion and exclusion criteria. Results Seven studies including 245 patients (107 receiving extended lesionectomy, 138 receiving lesionectomy) were selected. Meta-analysis and subgroup analyses were conducted to compare extended lesionectomy with lesionectomy. Pooled analysis demonstrated that seizure outcome was not statistically significantly improved in patients who underwent extended lesionectomy compared with lesionectomy (odds ratio = 0.77; 95% confidence interval, 0.39–1.51; P = 0.44; I 2 = 15%). Conclusions Extended lesionectomy does not contribute to better seizure control for patients with cerebral cavernous malformations with epilepsy. Resection of the lesion and surrounding hemosiderin is sufficient for patients with cerebral cavernous malformations presenting with epilepsy. Highlights • Extended lesionectomy versus lesionectomy was first compared by meta-analysis. • Extended lesionectomy does not contribute to better seizure control for patients with CCMs presenting with epilepsy. • Resection of lesion (malformed vessels) and surrounding hemosiderin is sufficient for patients with CCMs with epilepsy. [ABSTRACT FROM AUTHOR]

Background We tested the hypothesis that high-density lipoprotein (HDL) is associated with intracranial aneurysm growth and rupture. Methods We used an observational cohort study design. Age, sex, admission systolic blood pressure (SBP), diabetes, hypertension, coronary artery disease, aneurysmal rupture, apolipoprotein (APO)-A1, APO-B, HDL, low-density lipoprotein, triglycerides, cholesterol, and aneurysm location and size were recorded. Aneurysms <8 mm were categorized as small. Results The data from 581 patients with intracranial aneurysms were analyzed. The predictive factors for small size of aneurysms were female sex (odds ratio [OR], 0.630; 95% confidence interval [CI], 0.428–0.927; P = 0.019) and higher HDL (OR, 0.327; 95% CI, 0.159–0.672; P = 0.0002). In the subgroup of male patients, lower HDL was the only risk factor for large size (P = 0.015). The predictors of aneurysmal rupture were small size (OR, 0.875; 95% CI, 0.842–0.910; P = 0.000), higher HDL (OR, 3.716; 95% CI, 1.623–8.509; P = 0.002), no coronary artery disease (OR, 4.736; 95% CI, 1.528–14.681; P = 0.007), lower APO-A1 (OR, 0.202; 95% CI, 0.064–0.641; P = 0.007), and higher admission SBP (OR, 1.024; 95% CI, 1.015–1.032; P = 0.000). An HDL/aneurysm size ratio >0.31 was associated with a 46.2-fold increased likelihood of aneurysmal rupture (OR, 46.214; 95% CI, 13.386–159.548; P = 0.002). Conclusions The HDL level was inversely associated with intracranial aneurysm growth, especially in men. Higher HDL levels and small aneurysm size contributed to a greater risk of aneurysmal rupture. An HDL/size ratio >0.31 was a valuable predictor of intracranial rupture. Highlights • HDL levels were inversely associated with intracranial aneurysm growth. • Male sex showed a tendency toward increasing aneurysm size. • Higher HDL, small aneurysm, no CAD, lower APO-A1, and higher admission SBP increased aneurysmal rupture risk in our patients. • HDL/aneurysm ratio >0.31 is a valuable predictor of intracranial rupture. [ABSTRACT FROM AUTHOR]

Objective To study the anatomy and clinical application of monolateral pterional keyhole approaches for treating bilateral cerebral aneurysms. Methods Twelve formalin-fixed cadaveric heads underwent right pterional keyhole approaches for management of simulative contralateral aneurysms. The length of the contralateral middle cerebral artery (MCA), distal internal carotid artery (DICA), anterior cerebral artery, and ophthalmic segment of the internal carotid artery (OICA) was recorded. The operability of contralateral aneurysms was assessed using a modified numeric grading system. A total of 16 patients (12 patients with ruptured aneurysms) with bilateral cerebral aneurysms undergoing contralateral pterional keyhole approaches were included. Results The contralateral A1 segment of the anterior cerebral artery, proximal A2 segment, M1 segment of the MCA, DICA, and OICA was exposed via pterional keyhole approaches. An additional 2 mm of the OICA was exposed after incision of the falciform dural fold was completed. Contralateral aneurysms of the M1 segment (posterior), M2 segment, MCA bifurcation (inferior), A2 segment (lateral), DICA (posterior and lateral), and OICA (superior, inferior, and lateral) could not be fully exposed to perform simulated surgical clipping (operability rate <75%). A total of 36 aneurysms underwent adequate surgical clipping via unilateral pterional keyhole approaches, whereas 1 aneurysm of the A3 segment did not. Conclusions Contralateral aneurysms of the M1 segment (anterior, superior, and inferior), MCA bifurcation (superior and lateral), A1 segment, A2 segment (anterior, posterior, and medial), internal carotid artery bifurcation, DICA (anterior and medial), and OICA (medial) were fully exposed from different angles and surgical maneuvers were performed via pterional keyhole approaches, including in patients presenting with subarachnoid hemorrhage. [ABSTRACT FROM AUTHOR]

Summary Dysmorphic neurons and balloon cells constitute the neuropathological hallmarks of type II focal cortical dysplasias (FCDs) with refractory epilepsy. The genesis of these cells may be critical to the histological findings in type II FCD. Recent work has shown enhanced activation of the mTOR cascade in both balloon cells and dysmorphic neurons, suggesting a common pathogenesis for these two neuropathological hallmarks. A direct comparative analysis of balloon cells and dysmorphic neurons might identify a molecular link between balloon cells and dysmorphic neurons. Here, we addressed whether PDK1–AKT–mTOR activation differentiates balloon cells from dysmorphic neurons. We used immunohistochemistry with antibodies against phosphorylated (p)-PDK1 (Ser241), p-AKT (Thr308), p-AKT (Ser473), p-mTOR (Ser2448), p-P70S6K (Thr229), and p-p70S6 kinase (Thr389) in balloon cells compared with dysmorphic neurons. Strong or moderate staining for components of the PDK1–AKT–mTOR signaling pathway was observed in both balloon cells and dysmorphic neurons. However, only a few pyramidal neurons displayed weak staining in control group (perilesional neocortex and histologically normal neocortex). Additionally, p-PDK1 (Ser241) and p-AKT (Thr308) staining in balloon cells were stronger than in dysmorphic neurons, whereas p-P70S6K (Thr229) and p-p70S6 kinase (Thr389) staining in balloon cells was weaker than in dysmorphic neurons. In balloon cells, p-AKT (Ser473) and p-mTOR (Ser2448) staining was comparable with the staining in dysmorphic neurons. Our data support the previously suggested pathogenic relationship between balloon cells and dysmorphic neurons concerning activation of the PDK1–AKT–mTOR, which may play important roles in the pathogenesis of type II FCD. Differential expression of some components of the PDK1–AKT–mTOR pathway between balloon cells and dysmorphic neurons may result from cell-specific gene expression. [ABSTRACT FROM AUTHOR]

Summary Objectives In the winter of 2013, people were facing the risk of human-to-human transmission of the re-emerging influenza A(H7N9) virus. We report herein information on the clinical features of two patients from the same family infected with this virus, the genomic sequences of the viruses harbored, and antiviral drug sensitivity. Methods Clinical and epidemiological data of two patients from the same family were collected and analyzed. Sequencing was done for the viruses isolated from these two patients and one epidemiologically related chicken, and the sequences of the eight gene segments of the viruses were analyzed phylogenetically. The sensitivity of the viruses to antiviral drug treatment was determined by neuraminidase inhibitor susceptibility test. Results The two patients from one family cluster shared the same symptoms but had different outcomes, and had a strong epidemiological link. Three strains, two from these two patients and one from the chicken, were isolated. Genome sequencing and analyses of phylogenetic trees demonstrated that the two viruses were almost identical. We noted the presence of the PB2 E627K amino acid substitution that was not present in isolates from the first wave, as well as two new mutations in the NA gene and six in the PB2 gene. Drug sensitivity testing showed that the new isolates were resistant to oseltamivir but sensitive to peramivir. Conclusions The two patients from one family cluster were probable human-to-human transmission cases. The new isolates were sensitive to peramivir but showed reduced sensitivity to oseltamivir. [ABSTRACT FROM AUTHOR]