Pituitary apoplexy score, toward standardized decision-making: a descriptive study.

Pituitary apoplexy (PA), a rare and life-threatening complication of pituitary adenomas, prompts urgent glucocorticoid administration. The optimal surgical approach is debated, and the Pituitary Apoplexy Score (PAS) aids decision-making. Our retrospective study (2003-2022) assesses variables in PA patient groups (surgical vs. non-surgical), applying PAS to establish a significant threshold for surgical decisions. Additionally, we aim to compare the rates of ophthalmological and endocrine deficit between both groups and identify any associated variables. PAS discrepancies were observed, with averages of 1.7 ± 1.7 (p < 0.0001) for conservative and 3.9 ± 1.7 (p < 0.0001) for surgical groups, confirmed by multivariate analysis (p = 0.009). A PAS threshold of 5, showing over 80% positive predictive value, was established. Patients with low prolactin levels (< 5 ng/ml) had higher corticotropic deficiency prevalence at 3-month and 1-year follow-ups (p = 0.017 and 0.027). Our study supports PAS as a valuable PA management tool, suggesting potential variable adjustments. Multicenter studies are crucial due to PA's low incidence.

Extended endoscopic transsphenoidal approach for suprasellar craniopharyngiomas.

BACKGROUND: Craniopharyngiomas are benign sellar lesions. Surgical excision of craniopharyngiomas is difficult because of the surrounding important neurovascular structures. The choice of surgery depends on the histological type, location, hormonal status, and size of the craniopharyngioma, surrounding neurovascular structures, and invasion of the brain parenchyma. METHODS: We describe the resection of an adamantinomatous craniopharyngioma using an extended endoscopic endonasal approach and discuss the relevant surgical anatomy, indications, limitations, and possible complications. CONCLUSIONS: The extended endoscopic endonasal approach allows successful removal of the craniopharyngioma and poses little risk to surrounding neurovascular structures.

Surgical Site Infections after glioblastoma surgery: results of a multicentric retrospective study.

BACKGROUND: The effects of surgical site infections (SSI) after glioblastoma surgery on patient outcomes are understudied. The aim of this retrospective multicenter study was to evaluate the impact of SSI on the survival of glioblastoma patients. METHODS: Data from SSI cases after glioblastoma surgeries between 2009 and 2016 were collected from 14 French neurosurgical centers. Collected data included patient demographics, previous medical history, risk factors, details of the surgical procedure, radiotherapy/chemotherapy, infection characteristics, and infection management. Similar data were collected from gender- and age-paired control individuals. RESULTS: We used the medical records of 77 SSI patients and 58 control individuals. 13 were excluded. Our analyses included data from 64 SSI cases and 58 non-infected glioblastoma patients. Infections occurred after surgery for primary tumors in 38 cases (group I) and after surgery for a recurrent tumor in 26 cases (group II). Median survival was 381, 633, and 547 days in patients of group I, group II, and the control group, respectively. Patients in group I had significantly shorter survival compared to the other two groups (p < 0.05). The one-year survival rate of patients who developed infections after surgery for primary tumors was 50%. Additionally, we found that SSIs led to postoperative treatment discontinuation in 30% of the patients. DISCUSSION: Our findings highlighted the severity of SSIs after glioblastoma surgery, as they significantly affect patient survival. The establishment of preventive measures, as well as guidelines for the management of SSIs, is of high clinical importance.

Relevance of emergency head CT scan for fall in the elderly person.

OBJECTIVES: Fall of the elderly person is a public health problem. The objectives of our study were to evaluate the relevance of systematically performing in emergency a computed tomography (CT) scan for fall in the elderly person, to identify specific criteria predicting the appearance of lesions. MATERIAL AND METHODS: We performed a retrospective analysis of 500 consecutive patients aged 65 and over, who underwent an emergency head CT scan for fall from their height. Outcome at the end of the acute care, clinico-biological data and delays between trauma an d CT were collected, and crossed with a detection of head lesion on the CT scan. RESULTS: Of 500 patients, 38 (7.6%) had traumatic lesions depicted on the CT scan and 267 (53.4%) were hospitalized after the CT scan. Three (0.6%) had been operated for urgent head surgery. Nine of the 38 (23.6%) patients with traumatic lesion returned home. Presence of a lesion depicted on the CT scan was not correlated with the orientation of the patient (P < 0.0001). Post-traumatic injury was significantly associated with male sex (RR = 2.19, P = 0.0217), consciousness impairment (RR = 1.56, P < 0.0001), focal neurological deficit (RR = 6.36, P = 0.0362) and past history of post-traumatic brain injury (RR = 7.17, P = 0.0027). Anticoagulant therapy was not associated with increased risk of traumatic lesions (P = 0.3315). ROC analysis determined that a 5-hours time-interval between head trauma and CT allowed optimal detection of lesions. CONCLUSION: The systematic indication of an emergency head CT scan for fall in elderly patients presents a low diagnostic and therapeutic yield and is not relevant. Male sex, consciousness impairment, focal neurological deficit, past history of post-traumatic brain injury and time-interval between head trauma and CT are statistically related to the presence of lesions and should therefore be taken into account.

Pre-surgical embolization of intracranial meningioma with Onyx: A safety and efficacy study.

BACKGROUND AND PURPOSE: Pre-surgical embolization of large intracranial meningioma has been demonstrated to decrease blood loss and to improve the resectability of the tumor. Few reports have evaluated the risk and benefits of using Onyx in this indication. The objective of our study was to assess the efficiency and safety of pre-surgical embolization in a consecutive series of intracranial meningioma using Onyx. MATERIALS AND METHODS: We conducted a retrospective study of consecutive patients treated from 2010 to 2018 with pre-surgical embolization with Onyx for intracranial histologically-proven meningioma. Safety was evaluated by a report of the complications related to the procedure while efficacy was assessed on angiographic and histopathologic criteria. RESULTS: Forty-four meningioma in 44 patients treated with pre-surgical embolization were included in this study. Proximal artery occlusion was obtained in 97.6% (41/42) of the cases and good intra-tumoral penetration was achieved in 75.6% (31/41). Embolic agent inside blood vessels was identified in 63.5% (28/44) of cases. Embolization-induced necrosis was present in 79.6% (35/44) of cases. Six complications have been encountered (13.6%); 3 were stated as minor complications (6.8%) and 3 as major occurring in case of trans-ophthalmic route (6.8%). CONCLUSIONS: The present work is to date the largest study to evaluate intracranial meningioma embolization using Onyx. Onyx's allowed good intra-tumoral penetration and proximal artery occlusion in most cases but carries a higher risk of complication in case of ophthalmic supply.

Analysis of CDKN2A gene alterations in recurrent and non-recurrent meningioma.

PURPOSE: Assessment of the risk of recurrence is essential to determine the therapeutic strategy of meningioma treatment. Many relapsing or aggressive meningiomas show elevated mitotic and/or Ki67 indices, reflecting cell cycle deregulation. As CDKN2A is a key tumor suppressor gene involved in cell cycle control, we investigated whether CDKN2A alterations may be involved in tumor recurrence. METHODS: We carried out a comparative analysis of 17 recurrent and 13 non-recurrent meningiomas. CDKN2A single nucleotide variations (SNVs), deletions, methylation status of the promotor, and p16 expression were investigated. Results were correlated with the recurrent or non-recurrent status and clinicopathological data. RESULTS: We identified a CDKN2A SNV (NM_000077, exon2, c.G442A, p.Ala148Thr) in five meningiomas that was significantly associated with recurrence (p = 0.03). This mutation, confirmed by Sanger sequencing and referenced in the COSMIC database in various cancers, has not been reported in meningioma. The presence of one of the three following CDKN2A alterations-p.(Ala148Thr) mutation, whole homozygous or heterozygous gene loss, or promotor methylation > 8%-was observed in 13 of the 17 relapsing meningiomas and was strongly associated with recurrence (p < 0.0001) and a Ki67 labeling index > 7% (p = 0.004). CONCLUSION: We report an undescribed p.(Ala148Thr) CDKN2A mutation in meningioma that was only present in relapsing tumors. In our series, CDKN2A gene alterations were only found in recurrent meningiomas. However, our results need to be evaluated on a larger series to ensure that these CDKN2A alterations can be used as biomarkers of recurrence in meningioma.

MRI predictive score of pial vascularization of supratentorial intracranial meningioma.

OBJECTIVE: Meningiomas are highly vascularized tumors which may recruit pial blood supply. Pial supply complicates tumor treatment in numerous ways. The objective of this study was to establish a reliable MRI-based diagnostic score to predict the existence of pial blood supply in supratentorial intracranial meningiomas and then correlate the score with clinical and surgical outcomes and histopathological findings. METHODS: We performed a retrospective analysis of supratentorial histologically proven meningiomas in our institution from 2010 to 2018. A score was built based on MRI criteria and correlated with digital subtraction angiography (DSA) pial vascularization assessment. The score was then validated on a second independent population recruited with the same modalities. RESULTS: Logistic regression identified four parameters related to pial blood supply which were used to build the score: skull base location, tumor size > 45 mm, peritumoral flow voids, and incomplete cerebrospinal fluid rim. The overall diagnostic performance in predicting pial blood supply was as follows: sensitivity 97.8%, specificity 76.9%, predictive positive value 88.2%, negative predictive value 95.2%, and accuracy 90.3%. Inter-reader agreement and Cohen's kappa were good, respectively, of 90.7% and 0.69. A high score was associated with aggressive meningioma (World Health Organization II-III) (p = 0.04) and with greater importance of pial supply relative to dural supply. CONCLUSIONS: We have identified a reliable way to use MRI to predict the existence of pial blood supply in supratentorial intracranial meningiomas. A higher score also predicted higher grade meningioma. KEY POINTS: • Accurate and reproducible MRI score composed of four items to predict the existence of pial blood supply in supratentorial meningioma. • High score is associated with high-grade meningioma (WHO II-III) but also with greater importance of pial supply relative to dural supply.

Spontaneous regression of meningiomas after interruption of nomegestrol acetate: a series of three patients.

BACKGROUND: The relationship between increased meningioma incidence and growth and long-term hormonal therapy with cyproterone acetate (CPA) in women has been recently established in literature. Following the raise in awareness from hormonal treatment, we describe a potential relationship between the progesterone agonist nomegestrol acetate (NOMAC) and meningioma growth. METHODS: After implementation of a screening protocol to detect potential interactions between hormonal exposure and occurrence of meningioma, we identified patients taking NOMAC and newly diagnosed with a meningioma. NOMAC was stopped and those patients were followed tightly both clinically and radiologically. Retrospective volumetric analysis of the tumors was performed on the imaging. RESULTS: Three patients were identified for the study. After cessation of the NOMAC, tumor shrinkage was documented for all meningiomas within the first month. Up to 70% of tumor volume reduction was observed during the first year of follow-up in one of them. None of the patients developed new symptoms. CONCLUSION: We report the first cases of meningiomas responsiveness to discontinuation of hormonal therapy with NOMAC. Similarly to cases associated with long-term CPA intake, tumor reduction, and improvement of clinical symptoms can be observed after cessation of NOMAC.

Dual role of IL-21 in megakaryopoiesis and platelet homeostasis.

Gene profiling studies have indicated that in vitro differentiated human megakaryocytes express the receptor for IL-21 (IL-21R), an immunostimulatory cytokine associated with inflammatory disorders and currently under evaluation in cancer therapy. The aim of this study was to investigate whether IL-21 modulates megakaryopoiesis. We first checked the expression of IL-21 receptor on human bone marrow and in vitro differentiated megakaryocytes. We then investigated the effect of IL-21 on the in vitro differentiation of human blood CD34+ progenitors into megakaryocytes. Finally, we analyzed the consequences of hydrodynamic transfection-mediated transient expression of IL-21, on megakaryopoiesis and thrombopoiesis in mice. The IL-21Rα chain was expressed in human bone marrow megakaryocytes and was progressively induced during in vitro differentiation of human peripheral CD34+ progenitors, while the signal transducing γ chain was down-regulated. Consistently, the STAT3 phosphorylation induced by IL-21 diminished during the later stages of megakaryocytic differentiation. In vitro, IL-21 increased the number of colony-forming unit megakaryocytes generated from CD34+ cells and the number of megakaryocytes differentiated from CD34+ progenitors in a JAK3- and STAT3-dependent manner. Forced expression of IL-21 in mice increased the density of bi-potent megakaryocyte progenitors and bone marrow megakaryocytes, and the platelet generation, but increased platelet clearance with a consequent reduction in blood cell counts. Our work suggests that IL-21 regulates megakaryocyte development and platelet homeostasis. Thus, IL-21 may link immune responses to physiological or pathological platelet-dependent processes.

The P2X1 receptor is required for neutrophil extravasation during lipopolysaccharide-induced lethal endotoxemia in mice.

Extracellular ATP is becoming increasingly recognized as an important regulator of inflammation. However, the known repertoire of P2 receptor subtypes responsible for the proinflammatory effects of ATP is sparse. We looked at whether the P2X1 receptor, an ATP-gated cation channel present on platelets, neutrophils, and macrophages, participates in the acute systemic inflammation provoked by LPS. Compared with wild-type (WT) mice, P2X1(-/-) mice displayed strongly diminished pathological responses, with dampened neutrophil accumulation in the lungs, less tissue damage, reduced activation of coagulation, and resistance to LPS-induced death. P2X1 receptor deficiency also was associated with a marked reduction in plasma levels of the main proinflammatory cytokines and chemokines induced by LPS. Interestingly, macrophages and neutrophils isolated from WT and P2X1(-/-) mice produced similar levels of proinflammatory cytokines when stimulated with LPS in vitro. Intravital microscopy revealed a defect in LPS-induced neutrophil emigration from cremaster venules into the tissues of P2X1(-/-) mice. Using adoptive transfer of immunofluorescently labeled neutrophils from WT and P2X1(-/-) mice into WT mice, we demonstrate that the absence of the P2X1 receptor on neutrophils was responsible for this defect. This study reveals a major role for the P2X1 receptor in LPS-induced lethal endotoxemia through its critical involvement in neutrophil emigration from venules.

Delayed-onset post-craniotomy headache responsive to botulinum toxin A: a case series.

We report here the case of four patients presenting with delayed-onset temporal pain after pterional craniotomy. They reported similar symptoms: attacks of pain over the temporal region, ipsilateral to the operative site, irradiating around the eye and lasting from 10 min to 1 h. All patients had hypertrophy of at least one part of the temporalis muscle. All responded dramatically to botulinum toxin A injection (25 to 50 Botox® units) into the temporalis muscle. We suggest that the headaches were caused by aberrant nerve regeneration following surgical injury to the frontal branch of the facial nerve.

A Rab11A/myosin Vb/Rab11-FIP2 complex frames two late recycling steps of langerin from the ERC to the plasma membrane.

A large body of knowledge relating to the constitution of Rab GTPase/Rab effector complexes and their impact on both membrane domain organization and overall membrane trafficking has been built up in recent years. However in the context of the live cell there are still many questions that remain to be answered, such as where and when these complexes assemble and where they perform their primary function(s). We describe here the dynamic processes that take place in the final steps of the Rab11A dependent recycling pathway, in the context of the membrane platform constituted by Myosin Vb, Rab11A, and Rab11-FIP2. We first confirm that a series of previously reported observations obtained during the study of a number of trafficking cargoes also apply to langerin. Langerin is a cargo molecule that traffics through Rab11A-positive membrane domains of the endosomal recycling pathway. In order to explore the relative dynamics of this set of partners, we make extensive use of a combinatory approach of Live-FRET, fast FRAP video, fast confocal and TIRF microscopy modalities. Our data show that the Myosin Vb/Rab11A/Rab11-FIP2 platform is spatially involved in the regulation of langerin trafficking at two distinct sites within live cells, first at the sorting site in the endosomal recycling compartment (ERC) where transport vesicles are formed, and subsequently, in a strict time-defined order, at the very late stage of docking/tethering and fusion of these langerin recycling vesicles to the plasma membrane.

HLA-DQA2 and HLA-DQB2 genes are specifically expressed in human Langerhans cells and encode a new HLA class II molecule.

The precise role of human epidermal Langerhans cells (LCs) in immune response is highly controversial. While studying the gene expression profile of these cells, we were intrigued to identify the HLA-DQB2 gene as potentially expressed in LCs. Despite a strong evolutionary conservation of their sequences, the concomitant expression of the poorly polymorphic HLA-DQA2/HLA-DQB2 genes, paralogous to the HLA-DQA1/HLA-DQB1 genes, has never been detected in any cell type. We confirmed by RT-PCR that the HLA-DQA2 and -DQB2 genes are both expressed in LCs, but not in monocyte-derived dendritic cells, or in blood CD1c(+) or plasmacytoid dendritic cells. The presence of the HLA-DQß2 chain in LCs could be demonstrated by Western blotting, whereas immunofluorescence revealed its localization in early endosomes. As in the case of other HLA class II molecules, the HLA-DQα2 and -DQß2 chains formed heterodimers that had to associate with the invariant chain to reach endosomal compartments. HLA-DQα2/ß2 heterodimers were expressed at the cell surface, where they could mediate staphylococcal superantigen stimulation of T cells. Interestingly, HLA-DQα2 and HLA-DQß1 chains formed mixed heterodimers which efficiently left the endoplasmic reticulum. These observations strongly suggest that the poorly polymorphic HLA-DQA2 and -DQB2 genes should be considered to be of immunological importance. The HLA-DQα2/ß2 molecules could influence the complexity of the repertoire of Ags presented by LCs.

Fine tuning by human CD1e of lipid-specific immune responses.

CD1e is a member of the CD1 family that participates in lipid antigen presentation without interacting with the T-cell receptor. It binds lipids in lysosomes and facilitates processing of complex glycolipids, thus promoting editing of lipid antigens. We find that CD1e may positively or negatively affect lipid presentation by CD1b, CD1c, and CD1d. This effect is caused by the capacity of CD1e to facilitate rapid formation of CD1-lipid complexes, as shown for CD1d, and also to accelerate their turnover. Similar results were obtained with antigen-presenting cells from CD1e transgenic mice in which lipid complexes are assembled more efficiently and show faster turnover than in WT antigen-presenting cells. These effects maximize and temporally narrow CD1-restricted responses, as shown by reactivity to Sphingomonas paucimobilis-derived lipid antigens. CD1e is therefore an important modulator of both group 1 and group 2 CD1-restricted responses influencing the lipid antigen availability as well as the generation and persistence of CD1-lipid complexes.

Crystal structure of human CD1e reveals a groove suited for lipid-exchange processes.

CD1e is the only human CD1 protein existing in soluble form in the late endosomes of dendritic cells, where it facilitates the processing of glycolipid antigens that are ultimately recognized by CD1b-restricted T cells. The precise function of CD1e remains undefined, thus impeding efforts to predict the participation of this protein in the presentation of other antigens. To gain insight into its function, we determined the crystal structure of recombinant CD1e expressed in human cells at 2.90-Å resolution. The structure revealed a groove less intricate than in other CD1 proteins, with a significantly wider portal characterized by a 2 Å-larger spacing between the α1 and α2 helices. No electron density corresponding to endogenous ligands was detected within the groove, despite the presence of ligands unequivocally established by native mass spectrometry in recombinant CD1e. Our structural data indicate that the water-exposed CD1e groove could ensure the establishment of loose contacts with lipids. In agreement with this possibility, lipid association and dissociation processes were found to be considerably faster with CD1e than with CD1b. Moreover, CD1e was found to mediate in vitro the transfer of lipids to CD1b and the displacement of lipids from stable CD1b-antigen complexes. Altogether, these data support that CD1e could have evolved to mediate lipid-exchange/editing processes with CD1b and point to a pathway whereby the repertoire of lipid antigens presented by human dendritic cells might be expanded.

Structural reorganization of the antigen-binding groove of human CD1b for presentation of mycobacterial sulfoglycolipids.

The mechanisms permitting nonpolymorphic CD1 molecules to present lipid antigens that differ considerably in polar head and aliphatic tails remain elusive. It is also unclear why hydrophobic motifs in the aliphatic tails of some antigens, which presumably embed inside CD1 pockets, contribute to determinants for T-cell recognition. The 1.9-Å crystal structure of an active complex of CD1b and a mycobacterial diacylsulfoglycolipid presented here provides some clues. Upon antigen binding, endogenous spacers of CD1b, which consist of a mixture of diradylglycerols, moved considerably within the lipid-binding groove. Spacer displacement was accompanied by F' pocket closure and an extensive rearrangement of residues exposed to T-cell receptors. Such structural reorganization resulted in reduction of the A' pocket capacity and led to incomplete embedding of the methyl-ramified portion of the phthioceranoyl chain of the antigen, explaining why such hydrophobic motifs are critical for T-cell receptor recognition. Mutagenesis experiments supported the functional importance of the observed structural alterations for T-cell stimulation. Overall, our data delineate a complex molecular mechanism combining spacer repositioning and ligand-induced conformational changes that, together with pocket intricacy, endows CD1b with the required molecular plasticity to present a broad range of structurally diverse antigens.

Embolization of the middle meningeal artery for the prevention of chronic subdural hematoma recurrence in high-risk patients: a randomized controlled trial-the EMPROTECT study protocol.

BACKGROUND: Middle meningeal artery (MMA) embolization has been proposed as a treatment of chronic subdural hematoma (CSDH). The benefit of the procedure has yet to be demonstrated in a randomized controlled trial. We aim to assess the efficacy of MMA embolization in reducing the risk of CSDH recurrence 6 months after burr-hole surgery compared with standard medical treatment in patients at high risk of postoperative recurrence. METHODS: The EMPROTECT trial is a multicenter open label randomized controlled trial (RCT) involving 12 French centers. Adult patients (≥18 years) operated for CSDH recurrence or for a first episode with a predefined recurrence risk factor are randomized 1:1 to receive either MMA embolization within 7 days of the burr-hole surgery (experimental group) or standard medical care (control group). The number of patients to be included is 342. RESULTS: The primary outcome is the rate of CSDH recurrence at 6 months. Secondary outcomes include the rate of repeated surgery for a homolateral CSDH recurrence during the 6-month follow-up period, the rate of disability and dependency at 1 and 6 months, defined by a modified Rankin Scale (mRS) score ≥4, mortality at 1 and 6 months, total cumulative duration of hospital stay during the 6-month follow-up period, directly or indirectly related to the CSDH and embolization procedure-related complication rates. CONCLUSIONS: The EMPROTECT trial is the first RCT evaluating the benefit of MMA embolization as a surgical adjunct for the prevention of CSDH recurrence. If positive, this trial will have a significant impact on patient care. TRIAL REGISTRATION NUMBER: NCT04372147.

Deciphering the role of CD1e protein in mycobacterial phosphatidyl-myo-inositol mannosides (PIM) processing for presentation by CD1b to T lymphocytes.

Lipids are important antigens that induce T cell-mediated specific immune responses. They are presented to T lymphocytes by a specific class of MHC-I like proteins, termed CD1. The majority of the described CD1-presented mycobacterial antigens are presented by the CD1b isoform. We previously demonstrated that the stimulation of CD1b-restricted T cells by the hexamannosylated phosphatidyl-myo-inositol (PIM(6)), a family of mycobacterial antigens, requires a prior partial digestion of the antigen oligomannoside moiety by α-mannosidase and that CD1e is an accessory protein absolutely required for the generation of the lipid immunogenic form. Here, we show that CD1e behaves as a lipid transfer protein influencing lipid immunoediting and membrane transfer of PIM lipids. CD1e selectively assists the α-mannosidase-dependent digestion of PIM(6) species according to their degree of acylation. Moreover, CD1e transfers only diacylated PIM from donor to acceptor liposomes and also from membranes to CD1b. This study provides new insight into the molecular mechanisms by which CD1e contributes to lipid immunoediting and CD1-restricted presentation to T cells.

Treatment of A3.2 and A2 traumatic thoracolumbar spine compression fractures using vertebral body stenting: a 63-patient series.

BACKGROUND: Percutaneous treatments for spinal injury are underused by neuroradiologists and spine surgeons, mainly owing to a lack of data on indications. OBJECTIVE: To assess the safety and efficacy of vertebral body stenting (VBS) for post-traumatic A3.2 and A2 fractures (Magerl classification) and determine the factors that influence the improvements. METHODS: We retrospectively reviewed patients who underwent VBS to treat a single traumatic thoracolumbar fracture from 2010 to 2019. Kyphosis, loss of vertebral body height (VBH), and clinical and functional outcomes (including the Visual Analog Scale pain score and Oswestry Disability Index) were assessed. We examined the overall effects of VBH in all patients by constructing a linear statistical model and evaluated whether the efficacy was dependent on the characteristics of the patients or fractures. RESULTS: We included 63 patients comprising 44 A3.2 and 19 A2 fractures. No patient had worsening neurological symptoms or wound infection. The average rates of change were 67.1% (95% CI 59.1% to 75%) for kyphosis and 88.5% (95% CI 85.6% to 91.3%) for VBH (both p<0.0001). After 1 year, the VBS treatment was more effective for kyphosis in younger patients and at the L1 level, and for VBH in younger patients and cases of Magerl A3.2 fracture. CONCLUSIONS: This large reported series on VBS validates this surgical treatment. All patients had improved kyphosis and restored VBH. We recommend using VBS rather than open surgery for A3.2 and A2 fractures at the thoracolumbar junction and in young patients.