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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.

To retrospectively analyze the relationship between fibrinogen levels and outcomes in poor-grade aneurysmal subarachnoid hemorrhage (aSAH).We recruited 66 patients with poor-grade aSAH who were treated by neurosurgical clipping between January 2010 and December 2015. Serum samples were taken immediately on admission. Baseline information, complications, and outcomes at 6 months were recorded. Univariate and multivariate logistic regression analyses were used to explore the relationship between fibrinogen levels and clinical outcomes.Nineteen men and 47 women were included; the average age was 57.2 years. The median of the admission serum fibrinogen level was 3.3 g/L. Of the 66 patients, 18 had died by 6 months after initial hemorrhage, whereas 48 patients survived. Multivariate analyses showed that Hunt and Hess grade V (odds ratio [OR], 3.89; 95% confidence interval [CI], 1.06-14.20; P = 0.04) and admission serum fibrinogen level2.5 g/L (OR, 6.15; 95% CI, 1.67-22.67; P = 0.006) were significantly associated with 6-month mortality. In addition, admission serum fibrinogen level was negatively correlated with delayed cerebral ischemia, and admission serum fibrinogen level2.5 g/L (OR, 3.86; 95% CI, 0.99-15.09; P = 0.05) was also significantly associated with delayed cerebral ischemia.Patients with poor-grade aSAH with reduced admission fibrinogen level have a higher risk of delayed cerebral ischemia and 6-month mortality compared with those without. The admission serum fibrinogen level might be useful as a predictor and treatment target in patients with poor-grade sSAH who have undergone surgical treatment.

Parasitoids may deposit a second clutch of eggs on a host that has been parasitized by the same parasitoid species. This is termed “superparasitism”. Wolbachia infection increases the superparasitism frequency of Trichogramma females. We investigated the outcome and fitness cost of inter-strain intrinsic competition between Wolbachia-infected thelytokous strain (TDW) and uninfected bisexual strain (TDB) of Trichogramma dendrolimi. To determine the developmental rate of both strains, the size of immature stages of T. dendrolimi offspring at different times after parasitization was measured in single parasitism and superparasitism conditions. The results showed increased superparasitism by Wolbachia-infected females compared to uninfected females, regardless of the time interval between oviposition; Trichogramma females were unable to distinguish between host eggs previously parasitized by TDB or TDW females. When the first oviposition was performed by TDB females, the TDB offspring outcompeted TDW offspring deposited later. However, although the TDW offspring was deposited 8 h earlier than the TDB offspring, it gained no advantage over TDB offspring. Regardless of parasitism conditions, the differences in development rate and time between TDW and TDB offspring were not significant. This study revealed that albeit TDW females presented a higher tendency of superparasitism than TDB females, TDB offspring outcompeted TDW offspring even when the latter was deposited 8 h earlier. The negative effects of Wolbachia infection on the competitive ability of TDW offspring inside the host eggs were due to offspring’s low fitness rather than delayed development.

Parkinson's disease (PD) is the second most common neurodegenerative disorder and is characterized by severe neuronal loss. Necroptosis, or programmed cell necrosis, is mediated by the receptor interacting protein kinase-1 and -3/mixed lineage kinase domain-like protein (RIP1/RIP3/MLKL) pathway, and is involved in several neurodegenerative diseases. Here we aimed to explore the involvement of necroptosis in 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine hydrochloride (MPTP)-induced PD and determine the potential mechanisms. We found that the protein levels of RIP1, RIP3, and MLKL increased significantly in a MPTP-induced mouse PD model. High expression of RIP1/RIP3/MLKL was associated with severe loss of dopaminergic neurons. Pretreatment with necrostatin-1 or the knockout of the RIP3/MLKL gene to block necroptosis pathway dramatically ameliorated PD by increasing dopamine levels and rescuing the loss of dopaminergic neurons, independent of the apoptotic pathway. Moreover, upregulation of inflammatory cytokines in MPTP-treated mice was partially inhibited by deletion of RIP3 or MLKL gene, indicating that a positive feedback loop exists between these genes and inflammatory cytokines. Our data indicate that RIP1/RIP3/MLKL-mediated necroptosis is involved in the pathogenesis of MPTP-induced PD. Downregulating the expression of RIP1, RIP3, or MLKL can significantly attenuate MPTP-induced PD. Future therapy targeting necroptosis may be a promising new option.

Background and Purpose— Hypoxic-ischemic brain damage is a well-recognized physiopathologic mechanism after aneurysmal subarachnoid hemorrhage (aSAH). The Ngb (neuroglobin) is a hemoprotein predominantly expressed in the brain with a high affinity for oxygen. Relationship between serum Ngb level and brain metabolism in aSAH patients has not been investigated previously. Methods— Thirty-six consecutive severe aSAH patients (Glasgow Coma Scale score ≤8 on admission) with multimodal neuromonitoring and 36 matched healthy subjects were included. Serum Ngb level was analyzed in combination with other time-matched cerebral microdialysis parameters, brain tissue oxygen tension, and 12-month neurological outcomes. Results— Serum Ngb level was correlated positively with cerebral microdialysis parameters and brain tissue oxygen tension ( P 3) 12 months after aSAH was associated with higher Ngb level but independent of age, sex, and disease severity ( P P Conclusions— Ngb may be a potential biomarker for reflecting brain tissue oxygen tension, brain metabolism, and functional outcome in severe aSAH patients and merits further study in the context of aSAH.

Objective: We assessed the correlation between lactate dehydrogenase(LDH) to phosphate ratio and the prognosis of microsurgically clipping for ruptured intracranial aneurysm (rIA) in this study, to test the hypothesis that serum LDH to phosphate ratio could be a predictor for the outcome of microsurgically clipping for rIA. Methods: The rIA patients between 2012 and 2018 were retrospectively collected. Age, sex, Hunt-Hess(H-H) grade, Fisher grade, smoking, drink, medical history, aneurysm location, hydrocephalus, laboratory data including serum LDH, phosphate and LDH to phosphate ratio, related complication and the outcomes in 3 months were recorded. Results: A total of 1608 rIA patients in our institution were collected, and 856 patients treated by microsurgical clipping were enrolled. A significantly higher LDH- phosphate ratio on admission was observed in patients with poor outcome at 3 months (median±SD, 200.175±107.290 for mRS 0–2 vs 323.826±219.075 for mRS score 3–6; P Conclusions: LDH to phosphate ratio was a potential biomarker and could predict the unfavorable outcome of microsurgically clipping for rIA in 3 months. However, the detailed mechanism remain unclear and the conclusion needs be further confirmed by large-scale randomized clinical trials.

We explored the clinical significance of serum LDH level in aSAH patients after microsurgical clipping in our single institution, to test the hypothesis that higher serum LDH level predicts the outcome of aSAH patients at 3 months. A total of 2054 aSAH patients were collected, and 874 patients treated by microsurgical clipping were enrolled. And the serum LDH level within 24 hours after aSAH were recorded. The median serum LDH level (U/L) in the good outcome group (180.096±50.237) was obviously lower than that in the poor outcome group (227.554±83.002)(p=0.000). The area under the receiver operating characteristic (ROC) curve was 0.702(95% confidence interval [CI], 0.650 - 0.754; p=0.000). The optimal cutoff value for serum LDH level as a predictor for 3-month poor outcome (mRS>2) was determined as 201.5U/L in the ROC curve. Our finding showed that that higher serum LDH level correlated with Hunt & Hess grade, Fisher grade and neurological functional outcome, and predicted the outcome of aSAH at 3 months, which was involved in the related mechanisms of early brain injury and showed its great clinical significance in aSAH patients.

IntroductionThe treatment decision and long-term outcomes of previously untreated cerebral cavernous malformation (U-CCM) are still controversial. Therefore, we are conducting a nationwide multicentre prospective registry study in China to determine the natural history and effect of surgical treatment on long-term outcomes in Chinese people with U-CCM.Methods and analysisThis study was started on 1 January 2018 and is currently ongoing. It is a cohort follow-up study across a 5-year period. Patients will be followed up for at least 3 years after inception. Patients with U-CCM will be enrolled from 24 Grade III, level A hospitals distributed all over China. The cohort size is estimated to be 1200 patients. Patients are registered in surgically treated group and conservatively treated group. Clinical characteristics, radiology information and laboratory data are prospectively collected using an electronic case report form through an electronic data capture system. The primary outcome of this study is poor clinical outcome at the last follow-up (modified Rankin Scale score >2 lasting at least 1 year). The secondary outcome includes symptomatic haemorrhage, drug refractory epilepsy, focal neurological deficits, morbidity and all-cause mortality during follow-up. Univariate and multivariate regression analysis will be performed to determine the risk factors for poor outcomes in all patients, and to estimate the effect of surgery. Life tables, Kaplan-Meier estimates, log-rank test and proportional hazards Cox regression will be used to analyse the follow-up data of conservatively treated patients to determine the natural history of U-CCM. Initial presentation and location of U-CCM are prespecified subgroup factors.Ethics and disseminationThe study protocol and informed consent form have been reviewed and approved by the Research Ethical Committee of First Affiliated Hospital of Fujian Medical University (FAHFMU-2018-003).Written informed consent will be obtained from each adult participant or from the guardian of each paediatric participant. The final results will be published in peer-reviewed journals.Trial registration numberNCT03467295.

The relationships between lipoprotein-associated phospholipase A2 (Lp-PLA2) level, vasospasm, and clinical outcome of patients with aneurysmal subarachnoid hemorrhage (aSAH) are still unclear.To identify the associations between admission Lp-PLA2 and vasospasm following subarachnoid hemorrhage and the clinical outcome of aSAH.A total of 103 aSAH patients who had Lp-PLA2 level obtained within 24 h postbleeding were included. The relationships between Lp-PLA2 level, vasospasm, and clinical outcome were analyzed.Vasospasm was observed in 52 patients (50.49%). Patients with vasospasm had significantly higher Lp-PLA2 level than those without (P .001). Both modified Fisher grade (P = .014) and Lp-PLA2 level (P .001) were significant predictors associated with vasospasm. The Z test revealed that power of Lp-PLA2 was significantly higher than that of modified Fisher grade in predicting vasospasm (Z = 2.499, P = .012). At 6-mo follow-up, 44 patients (42.72%) had unfavorable outcome and 36 patients (34.95%) died. The World Federation of Neurosurgical Societies (WFNS) grade and Lp-PLA2 level were both significant predictors associated with 6-mo unfavorable outcome and mortality (all P .001). The predictive values of Lp-PLA2 for unfavorable outcome and mortality at 6-mo tended to be lower than those of the WFNS grade, but the differences were not statistically significant (P = .366 and 0.115, respectively). Poor-grade patients having Lp-PLA2 200 μg/L had significantly worse 6-mo survival rate than poor-grade patients having Lp-PLA2 ≤ 200 μg/L (P = .001).The Lp-PLA2 might be useful as a novel predictor in aSAH patients. A total of 30 poor-grade patients; those with elevated Lp-PLA2 level have higher risk of 6-mo mortality compared to those without.

Background The prevalence rates of freezing of gait (FOG) in Parkinson’s disease (PD) vary widely, ranging from 14.0 to 55.1%. Our aim is to calculate the overall prevalence of FOG in all PD patients with different disease durations and severities. Methods Using Medline/PubMed/Embase, we carried out a systematic literature search for studies reporting the PD and clinically relevant FOG. Results After primary screening, a total of 35 studies were identified and further analyzed for inclusion into the analysis, and 29 studies fulfilled the quality criteria and included in this meta-analysis. The overall prevalence of FOG in PD was 39.9% (95% CI 35.3-44.5%). The FOG identified by the freezing of gait questionnaire item 3 may be more prevalent (43.8%, 95% CI 38.5-49.1%) than the FOG identified by the Unified Parkinson’s Disease Rating Scale item 14 (36.0%, 95% CI 29.0-43.1%). Disease duration and severity are both the clinical features associated with the FOG. The highest FOG prevalence rate in PD patients was seen in patients with disease durations ≥ 10 years, at 70.8%, followed that of PD patients with disease durations ≥ 5 years (53.3%), and PD patients with disease durations < 5 years (22.4%). FOG presented in 28.4% of PD patients with Hoehn and Yahr staging (H&Y) score ≤ 2.5, and in 68.4% of PD patients with H&Y score ≥ 2.5. Conclusion This meta-analysis confirms that the prevalence of FOG in PD is considerable, and highlights the need for accurate identification of FOG in PD.

Rationale Glioblastoma is the most lethal and common malignant brain tumor but rare in patients with neurofibromatosis type 1. The clinical findings and pathological findings with gene signatures in female patients have not been well clarified. Patient concerns A 51-year-old female patient complained of headache and left limb weakness lasting for 20 days. The patient underwent a cesarean section 20 years ago and hysterectomy 1 year ago because of uterine leiomyomas. Multiple cafe-au-lait spots and neurofibromas were found over patient's chest, neck, back, and arms. The myodynamia of left distant and proximate epipodite were grade 0 and grade 1 respectively. The myodynamia of lower left limb was grade 3. Diagnoses Magnetic resonance imaging revealed a malignant lesion which was most likely a glioblastoma in the right temporo-parietal lobe, approximately 5.6 × 5.9 × 6.9 cm in size with a rounded boundary. Interventions A right temporo-parietal craniotomy was performed to resect the space-occupying lesion for gross total removal. Then, the patient received concurrent chemoradiotherapy. Histological examination confirmed a glioblastoma without v-RAF murine sarcoma viral oncogene homolog B1 gene, isocitrate dehydrogenase 1 gene, and telomerase reverse transcriptase gene promoter mutations. Outcomes After surgery, the headache was relieved and the muscular strength of left limbs did improve. After receiving the standard treatment regimen, the patient was alive at 13 months follow-up. Lessons This is the first reported glioblastoma in female neurofibromatosis type 1 patient without v-RAF murine sarcoma viral oncogene homolog B1 gene, isocitrate dehydrogenase 1 gene, and telomerase reverse transcriptase gene promoter mutations. Tumors in adult patients with these signatures were less aggressive with well-circumscribed border and had long-term survivals which strengthened the evidence that these patients may comprise a unique subset in glioblastoma.

OBJECTIVEGlutamate excitotoxicity and neuronal apoptosis are suggested to contribute to early brain injury after subarachnoid hemorrhage (SAH). Annexin A7 (ANXA7) has been shown to regulate glutamate release. However, the role of ANXA7 in early brain injury after SAH has not been illustrated. In this study, we aimed to investigate the effect of ANXA7 knockdown in reducing the severity of early brain injury after SAH, and determine the underlying mechanisms.METHODSEndovascular perforation was performed to induce SAH in male Sprague-Dawley rats. ANXA7-siRNA was administered via intraventricular injection 5 days before SAH induction. Neurological test, evaluation of SAH grade, assessment of blood-brain barrier (BBB) permeability, measurement of brain water content, Western blot, double immunofluorescence staining, TUNEL staining, and enzyme-linked immunosorbent assay (ELISA) were performed at 24 hours of SAH induction.RESULTSANXA7 protein expression increased significantly after SAH induction and was seen mainly in neurons. High expression of ANXA7 was associated with poor neurological status. ANXA7 knockdown dramatically ameliorated early brain injury through alleviating BBB disruption and brain edema. Further investigation of the mechanism showed that inhibiting ANXA7 expression can rescue neuronal apoptosis. In addition, ANXA7 knockdown also significantly reduced glutamate release, which was consistent with a significant increase of Bcl-2 expression and decreases of Bax and cleaved caspase-3 expression.CONCLUSIONSANXA7 can induce neuronal apoptosis by affecting glutamate release in rats with SAH. Downregulating the expression of ANXA7 can significantly attenuate early brain injury after SAH. Future therapy targeting ANXA7 may be a promising new choice.

OBJECTIVEThe relationship between lipoprotein-associated phospholipase A2 (Lp-PLA2) and various cardiovascular and cerebrovascular diseases is inconsistent. However, the connection between Lp-PLA2 level and delayed cerebral ischemia (DCI) following aneurysmal subarachnoid hemorrhage (aSAH) remains unclear. The objective of this study was to investigate the relationships between the Lp-PLA2 levels in the early stages of aSAH and the occurrence of DCI.METHODSThe authors evaluated 114 patients with aSAH who were enrolled into a prospective observational cohort study. Serum Lp-PLA2 level at admission (D0), on the first morning (D1), and on the second morning of hospitalization (D2) were determined using commercial enzyme-linked immunosorbent assay kits. The relationship between Lp-PLA2 levels and DCI was analyzed.RESULTSForty-three patients with aSAH (37.72%) experienced DCI. Mean serum Lp-PLA2 level decreased from 183.06 ± 61.36 μg/L at D0 (D0 vs D1, p = 0.303), to 175.32 ± 51.49 μg/L at D1 and 167.24 ± 54.10 μg/L at D2 (D0 vs D2, p = 0.040). The Lp-PLA2 level changes (D0-D1 and D0-D2) were comparable between patients with and without DCI. Multivariate model analysis revealed Lp-PLA2 level (D0) > 200 μg/L was a more significant factor of DCI compared with Lp-PLA2 (D1) and Lp-PLA2 (D2), and was a strong predictor of DCI (odds ratio [OR] 6.24, 95% confidence interval [CI] 2.05–18.94, p = 0.001) after controlling for World Federation of Neurosurgical Societies (WFNS) grade (OR 3.35, 95% CI 1.18–9.51, p = 0.023) and modified Fisher grade (OR 6.07, 95% CI 2.03–18.14, p = 0.001). WFNS grade (area under the curve [AUC] = 0.792), modified Fisher grade (AUC = 0.731), and Lp-PLA2 level (D0; AUC = 0.710) were all strong predictors of DCI. The predictive powers of WFNS grade, modified Fisher grade, and Lp-PLA2 (D0) were comparable (WFNS grade vs Lp-PLA2: p = 0.233; modified Fisher grade vs Lp-PLA2: p = 0.771). The poor-grade patients with Lp-PLA2 (D0) > 200 μg/L had significantly worse DCI survival rate than poor-grade patients with Lp-PLA2 (D0) ≤ 200 μg/L (p < 0.001).CONCLUSIONSThe serum level of Lp-PLA2 was significantly elevated in patients with DCI, and decreased within the first 2 days after admission. Lp-PLA2 in the early stages of aSAH might be a novel predictive biomarker for the occurrence of DCI.

Background Although coagulopathy have been proved to be a contributor to a poor outcome of aneurysmal subarachnoid hemorrhage (aSAH), the risk factors for triggering coagulation abnormalities have not been studied after aneurysm clipping. Methods We investigated risk factors of coagulopathy and analyzed the relationship between acute coagulopathy and outcome after aneurysm clipping. The clinical data of 137 patients with ruptured CA admitted to our institution was collected and retrospectively reviewed. Patient demographic data (age, sex), smoking, alcohol use, hypertension, diabetes, Hunt-Hess grade, Fisher grade, operation time, intraoperative total infusion volume, intraoperative blood loss, intraoperative transfusion, intraoperative hemostatic drug treatment, calcium reduction (preoperative free calcium concentration–postoperative free calcium concentration) were recorded. Coagulation was assessed within 24 h. Postoperative hemorrhage and infarction, deep venous thrombosis (DVT), and mortality were analyzed. Results Coagulopathy was detected in a total of 51 cases (group I), while not in 86 cases (group II). Univariable analysis demonstrated that age, smoking, alcohol use, intraoperative total infusion volume, intraoperative blood loss, intraoperative transfusion, and calcium reduction (≥ 1.2 mg/dl) were related to coagulopathy. Non-conditional logistic regression analysis showed that age [OR, 1.037 (95% CI, 1.001–1.074); p = 0.045] and calcium reduction (≥ 1.2 mg/dl) [OR, 5.509 (95% CI, 1.900–15.971); p = 0.002] were considered as the risk factors for coagulopathy. Hunt-Hess grade [OR, 2.641 (95% CI, 1.079–6.331); p = 0.033] and operation time [OR, 0.107 (95% CI, 1.012–0.928); p = 0.043] were considered as the risk factors for hypocoagulopathy. There were 6 cases (11.7%) with cerebral infarction in group I, while 6 cases (6.98%) in group II (χ 2 = 0.918, p = 0.338). There were 4 cases (7.84%) with rebleeding in group I, while 5 cases (5.81%) in group II (χ 2 = 0.215, p = 0.643). The mortality was 9.80% (5/51) in group I, while 1.16% (1/86) in group II (χ 2 = 5.708, p = 0.017). DVT was not detected in all cases. Conclusions In conclusion, age (≥ 65 years) and calcium reduction (≥ 1.2 mg/dl) were considered as the risk factors for coagulopathy and have been proved to be associated with higher mortality after aneurysm clipping.

Objective The underlying pathology of brain leading to cognitive impairment in Parkinson’s disease (PD) remains poorly understood. The aim of our study was to test the hypothesis that mild cognitive impairment (MCI) in PD may be related to atrophy of special gray matter regions. Methods High-resolution T1-weighted magnetic resonance images of the brains and comprehensive cognitive function tests were acquired in 37 PD patients and 21 healthy controls (HC) from September 2013 to October 2014. Patients were divided into two groups: PD with MCI (PD-MCI, n = 18) and PD with normal cognition (PDNC, n = 19). Gray matter density differences were analyzed using voxel-based morphometry (VBM). VBM and cognitive results, UPDRS scores and Hoehn–Yahr stages were compared between PD-MCI, PDCN and HC group, and correlation analyses were performed between those brain areas and cognition scores, UPDRS scores and disease duration, which showed significant group differences. Results The demographic data and motor severity among three groups were similar. However, comprehensive cognitive function results were more severe in PD-MCI than the other two groups. Compared to the HC group, the PDNC group showed reductions in gray matter density in frontal, temporal, parietal, bilateral insula lobes and many other regions of brain. Besides above changes, the PD-MCI group also revealed gray matter concentration decrease in left hippocampus and thalamus, and these changes still remained when compared with the PDNC group. The HC group did not show any more areas of atrophy in gray matter than others. Gray matter loss in PD represented significant correlations with global cognitive scores, motor severity or disease duration in some of these atrophic regions. Conclusion The initial stages of cognitive function decline in patients with PD is closely associated with gray matter atrophy in left hippocampus and thalamus. These two regions may serve as potential imaging biomarkers for PD-MCI.

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.

To study the anatomy and clinical application of monolateral pterional keyhole approaches for treating bilateral cerebral aneurysms.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.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 rate75%). A total of 36 aneurysms underwent adequate surgical clipping via unilateral pterional keyhole approaches, whereas 1 aneurysm of the A3 segment did not.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.

Background The multi-target deep brain stimulation (DBS) aimed at improving symptoms related to different nuclei is a promising research direction. However, to implant a single lead into multiple targets simultaneously is difficult with the current lead implantation method. New method We proposed a novel stereotaxic system used for implanting a curved lead to any two targets of the brain, and used the theoretical “curved lead method”. First, a customized novel stereotaxic system was fabricated, and a solid cranial model with six fixed internal targets was made; second, CT scan was performed to locate the fixed internal targets; third, five curved leads were implanted to five selected pairs of targets, each following the calculated parameters of “curved lead pathway” with the novel stereotaxic system, respectively. Finally, CT scans were performed again to determine the exact locations of the curved leads. Results The five curved leads accurately passed through the five pairs of combined targets, respectively, and the average vector error of curved lead implantation was 0.70 ± 0.24 mm. Comparison with Existing Method(s) In most situations, performing a multiple-target DBS procedure with the current stereotaxic systems means increased number of implanted leads, increased incidence of operative complications, and increased medical costs. However, the novel stereotaxic system could guide a single lead to reach two selected targets of the brain with high accuracy. Conclusions The novel stereotaxic system enables curved lead implantation with high accuracy, and can be considered as a useful complement to the current stereotaxic system.

Neuroglobin (Ngb) overexpression is considered as an intrinsic neuroprotective response. Therefore, exogenous Ngb increased in brain tissues has become a promising therapeutic strategy for neurological diseases. Previous studies demonstrated that transactivator of transcription (TAT) protein transduction domain was able to mediate synthetic Ngb entrance into neurons, and then protected brain from hypoxia-ischemic injury. However, the role of recombinant Ngb on early brain injury following subarachnoid hemorrhage (SAH) has not been elucidated. The objectives of this study were to investigate the expression of endogenous Ngb in brain using a rabbit model of SAH, and to verify whether TAT-Ngb fusion protein could be delivered into brain parenchyma, as well as to explore the neuroprotective effect of Ngb and its possible mechanisms. We found that Ngb expressions were up regulated in the transcript and protein levels in a similar time dependent manner after SAH as compared to the sham group. Moreover, TAT-Ngb fusion protein was successfully generated and transferred into brain neurons. Compared with the saline- and Ngb-treated group, neuronal viabilities and neurological outcomes were significantly improved 72 h post-SAH in the TAT-Ngb-treated group. Likewise, anti-apoptotic Bcl-2 protein was also elevated obviously. Conversely, pro-apoptotic factors including caspase 3, caspase 9 and Bax were greatly decreased after TAT-Ngb treatment. Our results suggest that Ngb plays a neuroprotective effect in rabbits suffering from SAH possibly through inhibiting the SAH-induced activation of mitochondria apoptotic pathway. Furthermore, TAT-mediated Ngb delivery into brain may be a promising therapeutic approach.

The basal ganglia-cortical circuits are important for information process to brain function. However, chronic recording of single-unit activities in the basal ganglia nucleus has not yet been well established. We present a movable bundled microwire array for chronic subthalamic nucleus (STN) single-unit electrocorticogram co-recording. The electrode assembly contains a screw-advanced microdrive and a microwire array. The array consists of a steel guide tube, five recording wires and one referenced wire which form the shape of a guiding hand, and one screw electrode for cortico-recording. The electrode can acquire stable cortex oscillation-driven STN firing units in rats under different behaving conditions for 8 weeks. We achieved satisfying signal-to-noise ratio, portions of cells retaining viability, and spike waveform similarities across the recording sections. Using this method, we investigated neural correlations of the basal ganglia-cortical circuits in different behaving conditions. This method will become a powerful tool for multi-region recording to study normal statements or movement disorders.