Search

Brain arteriovenous malformation (BAVM) is defined as abnormal communication between cerebral of arteries and veins, without capillaries. Clinically, it may involve intracranial hemorrhage or seizures. Complete spontaneous resolution, known as BAVM disappearance, has been reported in rare cases.We retrospectively collated all cases of BAVM in Lille University Hospital, from 2005 to 2018, and identified all cases of spontaneous BAVM disappearance on angiography (nidus and early venous drainage).There were 4 cases of spontaneous BAVM disappearance, in 3573 patients: i.e., prevalence of 0.1%. Sex ratio was 2:2; ages ranged from 14 to 46 years; nidus size was generally small (20mm); 3 of the 4 patients had superficial venous drainage. Revelation of BAVM was by hemorrhage in 3 cases and by seizure in 1. There were no cases of recanalization at 1 year's follow-up.Spontaneous BAVM disappearance is rare. Associated factors may include small nidus, superficial venous drainage and hemorrhage.

WHO grade II progestin-related meningiomas have been reported in recent series but we found no previous study describing their long-term outcome. Our study aimed to evaluate patients operated on for high-grade intracranial meningioma and who underwent long-term exposure to high dose of cyproterone acetate, nomegestrol acetate, and chlormadinone acetate. Our study retrospectively included 9 patients with high-grade progestin-related intracranial meningioma between December 2006 and September 2021. In each patient, clinico-radiological follow-up was performed every 6 months after diagnosis and treatment withdrawal recommendation. The mean progestative exposure was 11.4 years. Edema existence or absence of cleft sign on MRI were the key factors for surgical indication. All patients underwent surgery. Adjuvant radiotherapy was indicated in 1 patient, and Gamma Knife radiosurgery was proposed in 2 other patients for a second location of meningioma. Six patients harbored a grade II chordoid meningioma subtype with 100% PR expression and 3 patients a grade II atypical meningioma subtype with lower PR expression. The mean follow-up was 8.1 years and none of the 9 patients presented with a recurrence. Patients with grade II progestin-related meningiomas have less tumor recurrence after surgery than patients with sporadic grade II meningiomas, especially after progestin withdrawal. The presence/appearance of peri-meningioma edema and the absence of cleft sign before volumetric change should suggest the existence of an underlying WHO grade II meningiomas. In these cases, surgical resection may immediately be considered and adjuvant radiotherapy should be reserved for proven recurrence cases.

The relationship between meningioma and progestins has not been elucidated. Meningioma regression after acetate cyproterone (CA) withdrawal has been reported. Our purpose was to evaluate the meningioma evolution after withdrawal of progestins in patients who underwent long-term exposure to CA, nomegestrol acetate (NA), chlormadinone acetate (ChlA)., info:eu-repo/semantics/published

Introduction: High grade progestin related meningiomas have been reported in recent series but we found no previous study describing their long-term outcome. Our study aimed to evaluate patients operated on for high grade intracranial meningioma and who underwent long term exposure to high dose of cyproterone acetate, nomegestrol acetate and chlormadinone acetate.Methods: Our study retrospectively included 9 patients with high grade progestin related intracranial meningioma between December 2006 and December 2020. In each patient, clinico-radiological follow-up was performed every 6 months after diagnosis and treatment withdrawal recommendation. Results: The mean progestative exposure was 11.4 years. Edema existence or absence of cleft sign on MRI were the key factors for surgical indication. All patients underwent surgery. Ajduvant radiotherapy was indicated in 1 patient, and Gamma Knife Radiosurgery was proposed in 2 other patients for a second location of mengioma. 6 patients harbored a grade II chordoïd meningioma subtype with 100% PR expression and 3 patients a grade II atypical meningioma subtype with lower PR expression. The mean follow-up was 7.1 years and none of the 9 patients presented with a recurrence.Conclusion: Patients with Grade II progestin related meningiomas have less tumor recurrence after surgery than patients with sporadic high grade meningomas, especially after progestin withdrawal. The presence/ appearance of peri-meningioma edema and the absence of cleft sign before volumetric change should suggest the existence of an underlying high grade meningioma. In these cases, surgical resection may immediately be considered and adjuvant radiotherapy should be reserved for proven recurrence cases.

Internal variation among spheno-orbital meningiomas (SOM) is surgically challenging. Optic canal invasion management is discussed. This retrospective study includes 70 patients with SOM who underwent surgery between 1995 and 2012. Preoperative ophthalmological, neurological and aesthetic clinical signs were collected. All patients benefitted from repeated tomography and magnetic resonance imaging (MRI). The surgical team consisted of a neurosurgeon and a plastic surgeon. In the majority of cases, resection was followed by bone reconstruction using an autologous iliac crest graft. The extent of resection was evaluated on the dural and osseous sides. Early clinical outcomes, long-term follow-up, recurrence and adjuvant therapies were reported. The mean age was 52 years old, and 91 % of the patients were women. Initial symptoms primarily included proptosis (65 %), decreased visual acuity (39 %) and soft tissue tumefaction (16 %). We classified 40 cases as the internal variety when considering the inner third of the greater wing of the sphenoid, optic canal, anterior clinoid process or cavernous sinus. The remaining cases were described as the external variety. The complete resection rates for the internal and external varieties were 12 % and 61 %, respectively (P

Introduction Management of vertebral artery-posterior inferior cerebellar artery convergence (VA-PICA) saccular aneurysms requires a specialized neurovascular team. The objective is to preserve the functional outcome while performing a complete and reliable long-term exclusion of the aneurysm. Objective The aim of our study was to evaluate the outcome of patients with VA-PICA saccular aneurysms after treatment. Materials and methods This was a retrospective series of 21 consecutive patients with a VA-PICA saccular aneurysm treated between 2000 and 2012 at our institution. Treatment option (endovascular or microsurgical) was decided for each patient following a multidisciplinary discussion. Results Twenty-one patients were treated for a VA-PICA saccular aneurysm including 16 for a ruptured aneurysm and 5 for an asymptomatic aneurysm. Among all patients, 11 underwent endovascular treatment and 10 had microsurgical treatment. Our results showed a major aneurysm recurrence after endovascular treatment in 3 patients that required a further endovascular treatment in 2 cases. These 3 major recurrences occurred after treatment of a ruptured aneurysm when the initial angiography demonstrated the origin of the PICA at the neck of the aneurysm. After microsurgery, angiography showed a remnant neck in 2 patients including 1 treated by further endovascular procedure. Conclusion VA-PICA aneurysms are rare and require multidisciplinary management. Microsurgical treatment should be discussed when the PICA originates from the aneurysmal neck, particularly in patients with a ruptured small aneurysm, in order to obtain a reliable and long-term exclusion of the aneurysm.

Sensitive molecular assays have greatly improved the diagnosis of viral gastroenteritis. However, the proper preparation of stool samples for clinical testing remains an issue. bioMérieux has developed a stool preprocessing device (SPD) that includes a spoon for calibrated sampling and a vial containing buffer, glass beads, and two filters. The resulting stool filtrate is used for nucleic acid extraction. The purpose of this study was to evaluate the performance of the SPD for the quantification of human adenovirus (HAdV) DNA in stool samples collected from hematopoietic stem cell transplant (HSCT) recipients. HAdV DNA was quantified with the Adenovirus R-gene kit. The suitability of the device to reproducibly quantify HAdV DNA in stools using different extraction platforms (easyMAG and QIAsymphony) was determined using archived HAdV-positive stool samples. Coefficients of variation of HAdV DNA quantifications ranged from 1.79% to 1.83%, and no difference in quantification was observed between the two extraction systems. The HAdV DNA limit of quantification using the SPD was 3.75 log 10 copies/g of stool. HAdV DNA quantification using the SPD was then compared to that of the routine preprocessing technique on 75 fresh stool samples collected prospectively from pediatric HSCT recipients at risk for HAdV infections. Thirty-eight samples were HAdV DNA positive with both the SPD and routine preprocessing methods. HAdV DNA loads were on average 1.14-log 10 copies/g of stool higher with the SPD ( P < 0.0001) than with routine methods. This new device enabled a standardized preparation of stool samples in

International audience; BACKGROUND: Ruptured arteriovenous malformations (rAVM) are life-threatening diseases.OBJECTIVE: To evaluate the outcome of patients with grade 1 SPM rAVM after microsurgical treatment.METHODS: We retrospectively included 64 consecutive operated patients with a grade 1 SPM rAVM in our institution between 2002 and 2012. Complications related to the surgical procedure were recorded. All patients were re-evaluated 3months after treatment using the modified Rankin Scale score (mRS). Persistent neurological disorders were evaluated 1year after bleeding. Conventional cerebral angiography was performed for each patient immediately after surgical treatment and 1year later.RESULTS: The mean age at diagnosis was 30.8 years. Initial WFNS score was grade 1 in 25 patients, grade 2 in 11 patients, grade 3 in 10 patients, grade 4 in 9 patients and grade 5 in 9 patients. No remnant was left and a new surgery was performed only in a single patient who was initially operated-on under emergency conditions with limited preoperative investigations due to a poor clinical grade. Early postoperative complications related to the surgical procedure were recorded in 7 patients. The mRS score 3months after treatment was ≤2 in 53 patients (83%). Persistent neurological disorders were recorded in 40 patients (62.5%). High initial WFNS score (>2) and the hydrocephalus were significantly associated (P2).CONCLUSIONS: Grade 1 rAVM is a life-threatening disease concerning in most cases young patients. Long-term morbidity is often related to the hemorrhagic brain damage and rarely to the AVM resection.

OBJECTIVE Ruptured arteriovenous malformations (AVMs) are often obliterated after emergency microsurgical treatment. However, some studies have reported AVM recurrence after the obliteration of ruptured AVMs. The authors report their experience with AVM recurrence after successful microsurgical treatment of ruptured AVMs. METHODS The authors reviewed the medical data of 139 consecutive patients who underwent microsurgery at the authors' institution for ruptured AVM between 2002 and 2012. Each patient underwent a conventional cerebral angiography examination immediately after the surgery. Subsequent follow-ups were performed with MR angiography after 6 months, and, if there was no indication of AVM recurrence, patients were followed up with conventional cerebral angiography between 1 and 2 years after the treatment; pediatric patients were followed up until age 18 years. Recurrence was defined as new radiological evidence of an AVM at the site of a ruptured AVM or a new hemorrhage in patients with angiographically documented AVM obliteration on postoperative angiograms. RESULTS The mean age of the patients at the time of ruptured AVM diagnosis was 30.8 years (SD ± 5, range 4–69 years), and 44 of the patients were younger than 18 years (the mean age at diagnosis in this pediatric subgroup was 11.4 years [range 4–17.9 years]). Complete AVM obliteration after the initial microsurgery was observed in 123 patients (89.5%). Reappearance of an AVM was noted in 7 patients between 12 and 42 months after the treatment, and all of these patients were younger than 18 years. The recurrent AVM was located in an eloquent zone in 4 patients, and deep venous drainage was noted in 3 patients. Radiosurgery was performed in 6 of these patients, and 1 patient underwent another microsurgical procedure. The authors noted only one rebleeding due to an AVM recurrence during the latency period after radiosurgery. CONCLUSIONS The recurrence of an AVM is fairly rare and affects mostly pediatric patients. Therefore, especially in children, long-term angiographic follow-up is required to detect AVM recurrence or an AVM remnant. The authors stress the need for discussion involving a multidisciplinary neurosurgical team to decide on treatment in cases of any AVM recurrence or remnant.

Background Carotido-ophthalmic aneurysms are complex and their treatment is challenging. Few data are available on patient follow-up after endovascular or surgical treatment. Objective To evaluate outcome of patients with unruptured carotido-ophthalmic aneurysm after endovascular or surgical treatment. Materials and methods This series included 52 consecutive patients in a single center treated for an unruptured carotido-ophthalmic aneurysm at Lille University Hospital between 2000 and 2011. Visual disturbances were present in 5 patients. Treatment option (endovascular or microsurgical) was decided for each patient in a multidisciplinary meeting. We recorded age and the American Society of Anesthesiology score (ASA) before treatment and the modified Rankin Scale score (mRS) at 3 months after treatment. All patients had conventional angiography performed before and immediately after treatment. Long-term imaging follow-up was performed at 3 years after treatment. Results Treatment was endovascular in 29 patients and microsurgical in 23. The mean follow-up was 4.6 years. Conventional angiograms showed multiple intracranial aneurysms in 26 patients. Age, pre-therapeutic ASA score and mRS score at 3 months after treatment showed no significant difference between microsurgery and endovascular treatment. Imaging follow-up showed aneurysm recurrence after endovascular treatment in 6 patients including 3 with major recurrence that required further treatment by microsurgery. In these 3 major recurrences, the initial conventional angiography demonstrated the origin of the ophthalmic artery at the neck or from the aneurysmal sac in 3 cases. After microsurgery, conventional angiography showed a remnant neck in 2 patients including 1 treated by further endovascular procedure. Conclusion Endovascular treatment remains the first therapeutic option when the ophthamic artery originates at a distance from the neck, but microsurgery should be considered for large aneurysms with optic nerve compression, or when the ophthalmic artery arises from the neck of the aneurysm.

Objective: Cerebral accumulation of amyloid beta (A beta) is a pathological hallmark of Alzheimer's disease (AD). Proteolytic processing of amyloid precursor protein (APP) by alpha- or beta-secretase results in two soluble metabolites, sAPP alpha and sAPP beta, respectively. However, previous data have shown that both alpha- and beta-secretase have multiple cleavage sites. The aim of this study was to characterize the C-termini of sAPP alpha and sAPP beta in cerebrospinal fluid (CSF) by mass spectrometry (MS) and to evaluate whether different combinations of these fragments better separate between AD patients and controls by comparing two different sAPP immunoassays. Methods: Using immunoprecipitation and high resolution MS, the APP species present in CSF were investigated. CSF levels of sAPP alpha and sAPP beta from patients with AD (n=43) and from non-demented controls (n=44) were measured using AlphaLISA and MSD immunoassays that employ different antibodies for C-terminal recognition of sAPP alpha. Results: Four different C-terminal forms of sAPP were identified, sAPP beta-M671, sAPP beta-Y681, sAPP alpha-Q686, and 5APP alpha-K687 (APP770 numbering). Neither immunoassay for the sAPP species could separate the two patient groups. The correlation (R-2) between the two immunoassays was 0.41 for sAPP alpha and 0.45 for sAPP beta. Conclusion: Using high resolution MS, we show here for the first time that sAPP alpha in CSF ends at Q686 and K687. The findings also support the conclusion from several previous studies that sAPP alpha and sAPP beta levels are unaltered in AD. (C) 2013 Elsevier B.V. All rights reserved. (Less)

Cerebrospinal fluid (CSF) biomarkers for Alzheimer's disease (AD) reflect brain biochemistry. Using combined immunoprecipitation and mass spectrometry, we have shown that amyloid beta 1-15 (Aβ1-15) is produced by concerted β- and α-secretase cleavage of amyloid precursor protein (APP) and that the relative levels of Aβ1-16 in AD compared to controls are increased. Furthermore, drug-induced γ-secretase inhibition enhances the relative levels of Aβ1-15 and Aβ1-16. Here, we investigate a novel immunoassay for Aβ1-15/16 in a broad range of neurodegenerative conditions. The CSF level of Aβ1-15/16 was measured by the bead-based amplified luminescent proximity homogeneous assay (Alpha technology). Concentrations of Aβ1-15/16 were analyzed in subjects with Parkinson disease (PD; n = 90), PD with dementia (PDD) (n = 32), dementia with Lewy bodies (DLB) (n = 68), AD (n = 48), progressive supranuclear palsy (PSP) (n = 45), multiple system atrophy (MSA) (n = 46), and corticobasal degeneration (CBD) (n = 12). The detecting antibody is specific to the C-terminal epitope of Aβ15. We found that a carboxypeptidase (CPB) present in fetal bovine serum (FBS), a component of the buffers used, degrades Aβ1-16 to Aβ1-15, which is then detected by the Aβ1-15/16 assay. Significantly, lower levels of Aβ1-15/16 were detected in PD, PDD, PSP, and MSA compared to other neurodegenerative diseases and controls. Using the specific Aβ1-15/16 assay, a reliable quantification of Aβ1-15 or Aβ1-15/16 in CSF samples is obtained. We found reduced levels of Aβ1-15 in parkinsonian disease groups. The molecular mechanism behind this reduction is at present unknown.

Amyloid-β (Aβ) producing enzymes are key targets for disease-modifying Alzheimer's disease (AD) therapies since Aβ trafficking is at the core of AD pathogenesis. Development of such drugs might benefit from the identification of markers indicating in vivo drug effects in the central nervous system. We have previously shown that Aβ(1-15) is produced by concerted β-and α-secretase cleavage of amyloid-β protein precursor (AβPP). Here, we test the hypothesis that this pathway is more engaged upon γ-secretase inhibition in humans, and cerebrospinal fluid (CSF) levels of Aβ(1-15/16) represent a biomarker for this effect. Twenty healthy men were treated with placebo (n = 5) or the γ-secretase inhibitor semagacestat (100 mg [n = 5], 140 mg [n = 5], or 280 mg [n = 5]). CSF samples were collected hourly over 36 hours and 10 time points were analyzed by immunoassay for Aβ(1-15/16), Aβ(x-38), Aβ(x-40), Aβ(x-42), sAβPPα, and sAβPPβ. The CSF concentration of Aβ(1-15/16) showed a dose-dependent response over 36 hours. In the 280 mg treatment group, a transient increase was seen with a maximum of 180% relative to baseline at 9 hours post administration of semagacestat. The concentrations of Aβ(x-38), Aβ(x-40), and Aβ(x-42) decreased the first 9 hours followed by increased concentrations after 36 hours relative to baseline. No significant changes were detected for CSF sAβPPα and sAβPPβ. Our data shows that CSF levels of Aβ(1-15/16) increase during treatment with semagacestat supporting its feasibility as a pharmacodynamic biomarker for drug candidates aimed at inhibiting γ-secretase-mediated AβPP-processing.

Background:The ISAT and ISUIA studies, along with the improvement of endovascular treatment (EVT) have strongly influenced the management of intracranial aneurysms (IAs). We present our experience in the microsurgical treatment of unruptured IAs (UIAs) in this context.Methods:We retrospectively reviewed a consecutive series of non-giant UIAs selected for surgery during a five-year period. Patients and aneurysms characteristics, surgical results and outcome assessed by the Glascow Outcome Scale (GOS) at three month follow-up were studied.Results:Eighty-five patients underwent 93 surgical procedures to obliterate 113 UIAs. Those were incidental in 89% of the cases and mainly located on the middle cerebral artery (65%). Patients were assigned to surgery according to their medical history (young, previous subarachnoid haemorrhage), aneurysm characteristics (wide neck, branch at the neck, “small” size, associated “surgical” aneurysm) or failure of EVT (5%). Operatively, 48% of UIAs had thin wall or blebs and 71% were occluded with one titanium clip. Thrombectomy or temporary clipping were necessary in 4% and 11% of the cases, three aneurysms peroperatively ruptured, four were deemed unclippable, three paraclinoid UIAs had an intracavernous residue and 16% were wrapped because of a small neck remnant (class 2). The mortality rate was 0% and 4% of the patients experienced a definitive major neurological deterioration. Final GOS was unchanged in 96% of the patients.Conclusions:Despite reduction in operative cases and in appropriately selected patients ineligible to EVT, microsurgical clipping of non-giant anterior circulation UIAs can still achieve good outcome with very low mortality and neurological morbidity.

This study is a case report and review of the literature. Spinal cord herniation is a rare, although increasingly recognized, cause of spinal cord dysfunction. It is due to an anterior dural defect, through which the spinal cord herniates. The purpose of this article is to report the authors' experience and to provide insight on clinical presentation and radiological signs to make the reader aware of this entity and then to prevent misdiagnosis. The authors conducted a retrospective review of patients who underwent surgery for spinal cord herniation at their institution between 2000 and 2008. Three patients were treated (all women) and the interval between the onset of symptoms and surgery ranged from 24 to 48 months. All patients had progressive signs of thoracic myelopathy, and two of them were initially misdiagnosed. In all cases, the herniation was reduced and the defect repaired using different methods. The results and complications of our cases were compared with that of the reported literature. According to the results in these cases and the review of the literature, the authors believe that spinal cord herniation should be treated by using a dural patch to close the dural defect and to prevent retethering of the spinal cord.

Background and purpose Intracranial dural arteriovenous fistulas (DAVF) with cortical venous drainage are vascular malformations with high hemorrhagic risk. Their treatment may be complex and requires a multidisciplinary approach. Methods We retrospectively report 38 observations of dural arteriovenous fistulas with cortical venous drainage from 1990 to 2001. There were 28 men and 10 women with a mean age of 57 years. Hemorrhage revealed the malformation in 24 cases (63%). The other patients had headache, neurological deficit, seizure or pulsating mass of the scalp. One patient was asymptomatic. All the patients had DAVF with cortical venous drainage and decision of treatment was in each case multidisciplinary. Results Of the 38 patients, seven had no treatment for the following reasons: spontaneous occlusion of the malformation after hemorrhage, refusal of treatment, or poor neurological status at the admission. Thirty-one patients were treated and complete exclusion of the fistula was obtained in 30 cases. Endovascular occlusion of the fistula was performed in 14 patients, surgical clipping of the origin of the draining vein in 12 and combined treatment (surgical clipping after embolization of feeding arteries) in four. One patient had an untreated fistula despite several procedures. Conclusion Complete exclusion of these malformations is mandatory because of the potential risk of hemorrhagic complications. The best treatment is the occlusion of the origin of the draining vein (endovascular or surgical) and requires multidisciplinary discussion.

Objective Neurosurgical management of residual aneurysms (RA) after coiling remains a challenging issue. We present a consecutive series of 21 patients who underwent microsurgical treatment of a previously coiled aneurysm. Methods We retrospectively reviewed a consecutive series of 21 patients who underwent operations for an RA after coiling between 1997 and 2007. Postcoiling follow-up imaging included brain magnetic resonance angiography and digital subtraction angiography. The decision for surgical treatment was made when an RA was significant and unsuitable for re-embolization. Data related to the RA and to the surgical technique were analyzed. Postoperative outcome was evaluated with the Glasgow Outcome Scale. Results Twenty aneurysms were initially ruptured. Twelve had undergone complete coil occlusion, whereas 6 had a residual neck, 2 had a residual lobule, and 1 had a residual sac. The aneurysms were in the anterior circulation in 18 cases and in the posterior circulation in 3 cases. Twenty RAs were excluded with the apposition of 1 clip beneath the coils, 2 required a temporary occlusion, 2 required extraction of the coils, and 1 presented with an operative rupture. All aneurysms, except 2 that had their residual neck wrapped, were completely occluded. The postoperative Glasgow Outcome Scale score was unchanged in 90% of patients, and 2 patients sustained a moderate disability. Conclusion Microsurgical treatment of RA after endovascular treatment is effective, provided that patients are selected appropriately. The surgical treatment of recanalized aneurysms after coiling is challenging but can result in a good outcome with low morbidity and no mortality.

We report the case of a large dissecting aneurysm of the anterior cerebral artery revealed by cerebral infarction in 38-year-old man. The volume and aspect of the aneurysm initially led us to the diagnosis of saccular aneurysm. Given the complete thrombosis, the risk of bleeding was low and antithrombotic therapy was started. Surgery could be discussed later. However radiological monitoring by MRI (magnetic resonance imaging) showed a rapid decrease in volume of the aneurysm. The final angiography found an aspect of stenosis followed by a little arterial dilatation. The diagnosis of dissecting anterior cerebral aneurysm was a posteriori established.

International audience; OBJECTIVE: Our study aimed to evaluate the functional outcome and the risk of postoperative remnant in patients with rAVM after microsurgical treatment.METHODS: This is a retrospective of 139 consecutive patients operated for a rAVM between 2002 and 2012 in our institution. The age at diagnosis and the WFNS score were recorded for each patient before treatment. All patients were re-evaluated 3 months after treatment using mRS scale. Conventional angiography was performed in the first 2 postoperative weeks and then a year later to detect any remnant or recurrence.RESULTS: The mean age at diagnosis was 30.8 years (range 4-69 SD: ±5) and 44 patients had an age at diagnosis 2, SPM grade>2 and preoperative evaluation limited only to CT angiography in emergency situation (p

We aimed to evaluate the functional outcome and risk factors of recurrence in patients operated on for a chronic subdural hematoma (CSH), and discuss systematic early postoperative CT scans. CSH is a very common disease in neurosurgical practice, especially in elderly patients who are treated with anticoagulation. The challenge is to rapidly restore the independence of these patients. We retrospectively analyzed data from 164 consecutive surgical procedures performed on 140 CSH patients, including recurrent surgery, at our institution from June 2011 to June 2012. Pre- and postoperative CT scans, and medical records, were systematically reviewed using the institutional computing database. A poor functional outcome was defined by a modified Rankin scale (mRS) score>2 at 3 months. Among the 140 patients (mean age 76 years; 64% men), a single burr hole craniostomy was performed in 122 patients, and a craniotomy in 18. A poor functional outcome was recorded in 39 patients (28%; 95% confidence interval [CI] 20-35%). In multivariate analyses, an increased risk of poor functional outcome was associated with age >75 years (odds ratio [OR] 5.88; 95% CI 1.96-17.63), residual hematoma thickness >14 mm (OR 3.79; 95% CI 1.47-9.77), and GCS

Receptors of the scavenger class B family were reported to be localized in caveolae, the cell surface microdomains rich in free cholesterol and glycosphyngolipids, which are characterized by the presence of caveolin-1. Parenchymal hepatic and hepatoma HepG2 cells express very low levels of caveolin-1. In the present study, stable transformants of HepG2 cells expressing caveolin-1 were generated to address the effect of caveolin-1 on receptor activity. Compared to normal cells, these cells show higher (125)I-bovine serum albumin (BSA) uptake and cholesterol efflux, two indicators of functional caveolae. By immunoprecipitation, cell fractionation and confocal analyses, we found that caveolin-1 is well colocalized with the cluster of differentiation-36 (CD36) and the low-density lipoprotein (LDL) receptor (LDLr) but to a lesser extent with the scavenger receptor class B type I (SR-BI) in HepG2 cells expressing caveolin-1. However, caveolin-1 expression favors the dimerization of SR-BI. Two clones of cells expressing caveolin-1 were investigated for their lipoprotein metabolism activity. Compared to normal cells, these cells show a 71-144% increase in (125)I-LDL degradation. The analysis of the cholesteryl esters (CE)-selective uptake (CE association minus protein association) revealed that the expression of caveolin-1 in HepG2 cells decreases by 59%-73% LDL-CE selective uptake and increases high-density lipoprotein (HDL)-CE selective uptake by 44%-66%. We conclude that the expression of caveolin-1 in HepG2 cells moves the balance of LDL degradation/CE selective uptake towards degradation and favors HDL-CE selective uptake. Thus, in the normal hepatic parenchymal situation where caveolin-1 is poorly expressed, LDL-CE selective uptake is the preferred pathway.

1 Takahashi S, Suga T, Kawata Y, Sakamoto K: Anterior choroidal artery: angiographic analysis of variants and anomalies. AJNR Am J Neuroradiol 1990; 11: 719–729. 2 Takahashi M, Arii H, Tamakawa Y: Anomalous arterial supply of temporal and occipital lobes by anterior choroidal artery: angiographic study. AJNR Am J Neuroradiol 1980; 1: 537–540. 3 Von Mitterwallner F: Variationsstatistische Untersuchungen an den basalen Hirngefaessen. Acta Anat (Basel) 1955; 24: 51–87. 4 Chen C, Barkovich AJ: A hyperplastic anterior choroidal artery with double persistent anastamotic channels. AJNR Am J Neuroradiol 1998; 19: 1758–1760. 5 Buxton PJ, Cook PL: Anomalous origin of the parieto-occipital artery: case note. Neuroradiology 1993; 35: 212. 6 Furuno M, Yamakawa N, Okada M, Waga S: Anomalous origin of the calcarine artery. Neuroradiology 1995; 37: 658. 7 Blackburn IW: Anomalies of the encephalic arteries among the insane. J Comp Neurol Psychol 1907; 17: 493–517. Max Wintermark, University of California, San Francisco Department of Radiology, Neuroradiology Section 505 Parnassus Avenue, Box 0628 San Francisco, CA 94143-0628 (USA) Tel. +1 415 353 1639, Fax +1 415 353 8593 E-Mail Max.Wintermark@radiology.ucsf.edu Fig. 4. a Type 3 Takahashi anomaly. A hyperplastic AChorA supplies the parietooccipital and calcarine branches, while the PCA proper gives rise to the temporal branches. b Type 4 Takahashi anomaly. The PCA territory is almost completely fed by a hyperplastic AChorA arising from the ICA.

Introduction The safety and success of intracranial aneurysm (IA) surgery could be improved through the dedicated application of simulation covering the procedure from the 3-dimensional (3D) description of the surgical scene to the visual representation of the clip application. We aimed in this study to validate the technical feasibility and clinical relevance of such a protocol. Methods All patients preoperatively underwent 3D magnetic resonance imaging and 3D computed tomography angiography to build 3D reconstructions of the brain, cerebral arteries, and surrounding cranial bone. These 3D models were segmented and merged using Osirix, a DICOM image processing application. This provided the surgical scene that was subsequently imported into Blender, a modeling platform for 3D animation. Digitized clips and appliers could then be manipulated in the virtual operative environment, allowing the visual simulation of clipping. This simulation protocol was assessed in a series of 10 IAs by 2 neurosurgeons. Results The protocol was feasible in all patients. The visual similarity between the surgical scene and the operative view was excellent in 100% of the cases, and the identification of the vascular structures was accurate in 90% of the cases. The neurosurgeons found the simulation helpful for planning the surgical approach (ie, the bone flap, cisternal opening, and arterial tree exposure) in 100% of the cases. The correct number of final clip(s) needed was predicted from the simulation in 90% of the cases. The preoperatively expected characteristics of the optimal clip(s) (ie, their number, shape, size, and orientation) were validated during surgery in 80% of the cases. Conclusions This study confirmed that visual simulation of IA clipping based on the processing of high-resolution 3D imaging can be effective. This is a new and important step toward the development of a more sophisticated integrated simulation platform dedicated to cerebrovascular surgery.

Chronic hydrocephalus is a classic and recognized complication that affects 6 to 37% of patients with aneurysmal subarachnoid haemorrhage. The diagnosis is often mentioned due to the delayed onset of gait disturbance and slower psychomotor performance. The CT-scan confirms the diagnosis by showing an enlargement of the ventricles. In case of symptomatic hydrocephalus, a ventriculo-peritoneal shunt is often required. The authors report a rare case of chronic hydrocephalus presenting with visual symptoms, due to the delayed mobilisation of a surgical clip with direct mass effect over the anterior optic pathways. The treatment of hydrocephalus led to a rapid and complete regression of symptoms.

Introduction Pericallosal artery aneurysms (PAA) represent 2 to 9% of intracranial aneurysms and their management remains difficult. Objective We aimed to report our experience to evaluate the outcome of patients with ruptured and unruptured PAA, when the treatment modality is decided in a multidisciplinary fashion. Materials and methods In this retrospective study, we included 28 patients (8 men and 20 women) treated for a PAA in our institution between 2002 and 2012, among the 2430 patients who underwent the treatment of an intracranial aneurysm in the same period. Fifteen patients harbored a ruptured aneurysm while 13 benefited from a prophylactic treatment. The mean age at diagnosis was 52 years (range 37 to 75 SD: ±5) in patients with ruptured aneurysm and 54.2 years (range 35 to 66 SD: ±5) in patients with unruptured aneurysm. Endovascular treatment has been performed in 9 patients while 19 patients underwent a microsurgical treatment. Clinical outcome has been assessed using the modified Rankin scale (mRS) at 3 months. Long-term imaging follow-up included a CT angiography at 36 months for clipped aneurysms and MR angiography at 6, 18 and 36 months for coiled aneurysms. Results The median follow-up was 3.4 years (range 2.8 to 4.2). The mRS was ≤ 2 in all patients with unruptured aneurysms. In patients with ruptured aneurysm, the mRS was ≤ 2 at 3 months in 13 patients (87%). Persistent cognitive disorders were noted in 8 patients with ruptured aneurysm, 2 of them were considered as possibly related to the treatment. Aneurysm recurrence has been depicted in 4 patients (at 6 months in 3 patients and 1 year in 1 patient) requiring further treatment in all cases; all of them had an aneurysm remnant on immediate conventional angiography. No recurrence was noted in patients without remnant on immediate post-treatment angiography. Conclusion Both endovascular and microsurgical treatment are challenged in this location. Multidisciplinary discussion is essential to optimize the management of patients with PAA.

The study design involved case reports and review of the literature. Oncotic aneurysm from choriocarcinoma is an extremely rare event that should be known by all neurosurgeons and suspected in women of childbearing age. The purpose of this article is to report the authors' experience and to provide insight on clinical presentation and radiological signs to aware the reader to this entity and then to prevent misdiagnosis. The authors report two cases of ruptured oncotic aneurysm treated at their institution in 2010. A review of the literature was performed to discuss the pathogenesis and the role of the neurosurgeon. Chemotherapy is the treatment of choice making surgery necessary only for patients with large intracerebral haematoma that represents an immediate threat.

Vascular endothelial growth factor (VEGF) is an angiogenic and neurotrophic factor in both adult and neonatal animals, but its expression and role have been incompletely studied in the developing human brain. We analyzed the distribution of VEGF and its high-affinity receptor VEGFR-2 in the human forebrain and cerebellum at developmental stages from 14 weeks' gestation (WG) to the13th postnatal month. Tissue samples free of detectable neuropathologic abnormalities were assessed by immunohistochemistry and confocal microscopy using anti-human VEGF and VEGFR-2 antibodies. The VEGFR-2 was first expressed in the whole cerebral mantle and in migrating cells in the intermediate zone, whereas VEGFwas found in superficial layers of the cortical plate, in radial glia, and in the cerebellar external germinal cell layer. From 23 WG, temporospatial VEGFR-2 expression was superimposable on that ofVEGF in the cortical plate, intermediate zone, basal ganglia, limbicstructures, and external germinal cell layer. The VEGF/VEGFR-2-positive astrocytes were observed during their generation and migration from 23 WG to the first postnatal month. The VEGF-positive mature oligodendrocytes were observed in myelinating structures in the forebrain from birth and in the cerebellum from 24WG. These data suggest that VEGF and VEGFR-2 are likely involved in several aspects of human brain development.

The central hypothesis of excitotoxicity is that excessive stimulation of neuronal NMDA-sensitive glutamate receptors is harmful to neurons and contributes to a variety of neurological disorders. Glial cells have been proposed to participate in excitotoxic neuronal loss, but their precise role is defined poorly. In thisin vivostudy, we show that NMDA induces profound nuclear factor κB (NF-κB) activation in Müller glia but not in retinal neurons. Intriguingly, NMDA-induced death of retinal neurons is effectively blocked by inhibitors of NF-κB activity. We demonstrate that tumor necrosis factor α (TNFα) protein produced in Müller glial cells via an NMDA-induced NF-κB-dependent pathway plays a crucial role in excitotoxic loss of retinal neurons. This cell loss occurs mainly through a TNFα-dependent increase in Ca2+-permeable AMPA receptors on susceptible neurons. Thus, our data reveal a novel non-cell-autonomous mechanism by which glial cells can profoundly exacerbate neuronal death following excitotoxic injury.

Reliable real-time quantitative PCR assays to measure Epstein-Barr virus (EBV) DNA load (EBV) are useful for monitoring EBV-associated diseases. We evaluated a new commercial kit, EBV R-gene Quantification kit (Argene, Varilhes, France) to quantify EBV DNA load in whole blood. Assay performance was assessed with two PCR platforms (LightCycler 2.0 and SmartCycler 2.0) and three commercial DNA extraction methods. The assay was compared with our in-house real-time EBV PCR using samples from the Quality Control for Molecular Diagnostics 2006 EBV proficiency program and using 167 whole-blood specimens from individuals with infectious mononucleosis, from transplanted or HIV-infected patients, and from EBV-seropositive healthy carriers. The EBV R-gene assay was sensitive to 500 copies of EBV DNA per milliliter of whole blood with the two PCR platforms and the three extraction methods and was linear across 4 orders of magnitude. Intra- and interassay coefficients of variations were less than 20%. Nine of 10 samples tested with the EBV R-gene were in agreement with the expected qualitative results of the Quality Control for Molecular Diagnostics 2006 EBV proficiency program, and 7 of 10 samples were within ±0.5 log units of the expected quantitative values, with discrepant results mostly observed for low viral load (ie

Neuronal death due to excessive activation of N-methyl-d-aspartate (NMDA) receptors is a hallmark of neurodegenerative diseases. The polyamines: putrescine, spermine, and spermidine, bind to specific sites on the NMDA receptor and promote its activation, but their role in NMDA-induced neuronal death is ill defined. In this study, we characterized the role of polyamines in excitotoxic death of retinal ganglion cells (RGCs), a population of central neurons susceptible to NMDA-induced damage. Our data show that endogenous arginase I, the rate limiting enzyme for polyamine biosynthesis, is expressed in the intact, adult retina. Intraocular injection of NMDA visibly increased arginase I expression in Muller cells, the predominant glial cell-type in the mammalian retina. Inhibition of polyamine synthesis using di-fluoro-methyl-ornithine (DFMO) was markedly neuroprotective, while injection of exogenous polyamines in conjunction with NMDA exacerbated RGC death. Blockade of the polyamine binding sites on NMDA receptors using the non-competitive antagonist ifenprodil was neuroprotective, suggesting that polyamines contribute to excitotoxic death, at least partly, by binding to NMDA receptors. Importantly, we also demonstrate that NMDA leads to activation of both the Erk1/2 and PI3 K/Akt pathways, but only the PI3 K/Akt kinase was required for di-fluoro-methyl-ornithine-induced RGC survival. In summary, our study reveals that polyamines modulate neuronal death in the retina via different mechanisms that potentiate NMDA-triggered excitotoxicity.

Software designed to help the neurosurgeon in the diagnosis of shunt malfunction is presented. This software allows the possibility to record on a 3.5 diskette a patient's clinical information and four views of a CT scan performed when the patient was doing perfectly well with his shunt. This diskette, operated by MS-DOS on any IBM-compatible personal computer, can be read at any time, anywhere. The evaluation of the system demonstrated it was safe, with an excellent adhesion of the patients and of their families.

Plasma low- and high-density lipoproteins (LDL and HDL) are cleared from the circulation by specific receptors and are either totally degraded or their cholesteryl esters (CE) are selectively delivered to cells by receptors such as the scavenger receptor class B type I (SR-BI). The aim of the present study was to define the effect of apoC-II and apoC-III on the uptake of LDL and HDL by HepG2 cells. Stable transformants were obtained with sense or antisense strategies that secrete 47-294% the normal level of apoC-II or 60-200% that of apoC-III. Different levels of secreted apoC-II or apoC-III had little effect on LDL and HDL protein degradation by HepG2 cells. However, compared to controls, cells under-expressing apoC-II showed a 160% higher capacity to selectively take up HDL-CE, while cells under-expressing apoC-III demonstrated 70 and 160% higher capacity to take up CE from LDL and HDL, respectively. In experiments conducted with exogenously added apoC-II or apoC-III, no significant effect was observed on lipoprotein-protein association/degradation; however, LDL-CE and HDL-CE selective uptake was significantly reduced in a dose-dependent manner. These results indicate that apoC-II and apoC-III inhibit CE-selective uptake.