Explore the vast range of titles available.

Spinal tuberculosis is due to globalization no longer a disease limited to developing nations. It remains in Germany a rarity and still a difficult diagnosis. Here we analyzed patients with spinal tuberculosis treated at our neurosurgical department. According to the infected anatomic segment, patients were assigned in one of three groups. Surgery was performed when neurological deficit due to mechanical compression, deformity, instability, severe pain, necrotic bone or failure to respond to anti-tuberculous treatment were observed. We identified 34 patients with spinal tuberculosis who underwent surgical treatment. In the cervical spinal tuberculosis group, there were 15 cases (46.9%) In most cases treatment consisted of spinal instrumentation. In the thoracic group, 10 cases (29.4%) were observed. The treatment was performed by dorsolateral spinal instrumentation. For the thoracolumbar group, 9 cases (26.4%) were observed. In most cases dorsolateral spinal instrumentation was performed. One patient in the first group and one patient in the third group relapsed after operation. A second surgery was necessary. Patients with chronic back pain, immigration background and/or neurological deficit spinal TB should be considered as a differential diagnosis. Combined surgical intervention and medical treatment is associated with a favorable outcome.

Neuronal-glioma interactions are increasingly recognized as critical in the development and progression of central nervous system tumors. Recent research highlights that gliomas can integrate into neural circuits through various mechanisms, including the synaptogenic factor thrombospondin-1 (TSP-1). This new mechanistic understanding of cancer neuroscience allows for novel insights into target discovery. Critically, therapies that modulate neuron-tumor interactions remain agnostic to other oncogenic changes within tumor cells yet may still target fundamental drivers of tumor growth. In line with these findings and controlling for critical confounding variables, we demonstrate a survival benefit associated with gabapentin (an antagonist of TSP-1) following surgical resection of newly diagnosed glioblastoma. This retrospective, multi-institutional cohort study included 1,072 patients, with a discovery cohort of 693 patients and an additional 379 patients from a separate site for external validation. Furthermore, our findings indicate that gabapentin administration is associated with reduced serum TSP-1 levels, suggesting its potential as a future biomarker. In preclinical studies, the FDA approved TSP-1 antagonist gabapentin has been shown to disrupt neuronal-glioma interactions, slowing glioblastoma progression. Here, authors report a retrospective cohort study demonstrating a survival benefit associated with gabapentin in patients with newly diagnosed glioblastoma.

Glioblastoma is the most common and lethal central nervous system malignancy with a median survival after progression of only 6–9 months. Major biochemical mechanisms implicated in glioblastoma recurrence include aberrant molecular pathways, a recurrence-inducing tumor microenvironment, and epigenetic modifications. Contemporary standard-of-care (surgery, radiation, chemotherapy, and tumor treating fields) helps to control the primary tumor but rarely prevents relapse. Cytoreductive treatment such as surgery has shown benefits in recurrent glioblastoma; however, its use remains controversial. Several innovative treatments are emerging for recurrent glioblastoma, including checkpoint inhibitors, chimeric antigen receptor T cell therapy, oncolytic virotherapy, nanoparticle delivery, laser interstitial thermal therapy, and photodynamic therapy. This review seeks to provide readers with an overview of (1) recent discoveries in the molecular basis of recurrence; (2) the role of surgery in treating recurrence; and (3) novel treatment paradigms emerging for recurrent glioblastoma.

Oncolytic virotherapy is a rapidly progressing field that uses oncolytic viruses (OVs) to selectively infect malignant cells and cause an antitumor response through direct oncolysis and stimulation of the immune system. Despite demonstrated pre-clinical efficacy of OVs in many cancer types and some favorable clinical results in glioblastoma (GBM) trials, durable increases in overall survival have remained elusive. Recent evidence has emerged that tumor-associated macrophage/microglia (TAM) involvement is likely an important factor contributing to OV treatment failure. It is prudent to note that the relationship between TAMs and OV therapy failures is complex. Canonically activated TAMs (i.e., M1) drive an antitumor response while also inhibiting OV replication and spread. Meanwhile, M2 activated TAMs facilitate an immunosuppressive microenvironment thereby indirectly promoting tumor growth. In this focused review, we discuss the complicated interplay between TAMs and OV therapies in GBM. We review past studies that aimed to maximize effectiveness through immune system modulation—both immunostimulatory and immunosuppressant—and suggest future directions to maximize OV efficacy.

An inverse association between the use of platelet inhibitors and the risk of cancer has been reported by numerous epidemiological studies in the past. The effects of antiplatelet agents on the cerebral metastasis formation of non-small cell lung cancer (NSCLC) are largely unknown. We therefore, investigated the effect of platelet inhibition in NSCLC patients at the time of the first diagnosis of cerebral metastases. We retrospectively investigated the clinical course of 417 NSCLC patients with cerebral metastases who underwent craniotomy for metastasis resection during the course of their disease. The presence of platelet inhibition prior to cerebral metastases diagnosis was used to dichotomize the cohort. Relevant clinical parameters, time to neurosurgical intervention for cerebral metastases, overall survival, and the incidence of intracranial hemorrhage or hemorrhagic transformation of metastases, were compared between the two groups. The presence of platelet inhibitor intake was associated with a significantly prolonged time to neurosurgical intervention for cerebral metastases in non-small cell lung cancer 63 vs. 47 months; ( p  = 0.001). Furthermore, platelet inhibitor intake was also associated with an increased overall survival of 12 vs. 10 months ( p  = 0.02). Statistically, no increased risk of hemorrhagic transformation of the metastasis or intracranial hemorrhage was found ( p  = 0.635 and p  = 1.000), respectively. In this retrospective study, the use of platelet inhibitors was not associated with an increased risk of intracranial hemorrhage, the use of platelet inhibitors was associated with delayed need for neurosurgical treatment for cerebral metastases and improved overall survival in NSCLC patients.

Current guidelines suggest surgical decompression for ischemic cerebellar stroke in case of significant mass effect. Recent research has aimed to identify a possible threshold for mass effect. However, a computer-assisted volumetry in acute setting is time consuming and impracticable, wherefore the aim of this study was to assess the accuracy and clinical applicability of the ABC/2 method in case of ischemic cerebellar stroke. Imaging data of 125 patients, including preoperative CT or MRI scans were used for volumetric analysis. The ABC/2 formula using scans in axial and coronal planes. BrainLab® Elements software was used for computer assisted volumetry by defining the region of interest allowing automated volumetric calculation. Measurements were conducted independently by blinded clinicians. Pearson correlation and Bland-Altmann test were used for statistical analysis. Among the 125 cerebellar infarctions analyzed, there was no statistical difference of mean infarct volume measurement between the ABC/2 formula and computer-assisted volumetry (16.6mL vs. 15.91mL; range 0.8-67.7mL; p = 0.76). The Spearman correlation test indicated a strong correlation between the two methods (r = 0.985, 95% CI: 0.979-0.990, p < 0.0001). Discrepancies were most notable in smaller infarction volumes (<10 mL), prompting a subgroup analysis. For infarct volume less than 10mL, the ratio of volumetric differences ranged from 47% to 60%, with absolute volume differences from -3-3 mL whereas the ratio ranged from -20% to 29%, with absolute volume differences from -6-8 mL in cases with infarct volume greater equal 10mL. ABC/2 formula shows a good correlation with computer-assisted volumetry. Consequently, it could serve as a fast and practical tool for estimating cerebellar infarct volume and aiding decision-making in clinical practice. However, the limitations and variability of the ABC/2 method, particularly for smaller infarcts, must be considered.

PurposeNeuro-oncology tumor boards (NTBs) hold an established function in cancer care as multidisciplinary tumor boards. However, NTBs predominantly exist at academic and/or specialized centers. In addition to increasing centralization throughout the healthcare system, changes due to the COVID-19 pandemic have arguably resulted in advantages by conducting clinical meetings virtually. We therefore asked about the experience and acceptance of (virtualized) NTBs and their potential benefits.MethodsA survey questionnaire was developed and distributed via a web-based platform. Specialized neuro-oncological centers in Germany were identified based on the number of brain tumor cases treated in the respective institution per year. Only one representative per center was invited to participate in the survey. Questions targeted the structure/organization of NTBs as well as changes due to the COVID-19 pandemic.ResultsA total of 65/97 institutions participated in the survey (response rate 67%). In the context of the COVID-19 pandemic, regular conventions of NTBs were maintained by the respective centers and multi-specialty participation remained high. NTBs were considered valuable by respondents in achieving the most optimal therapy for the affected patient and in maintaining/encouraging interdisciplinary debate/exchange. The settings of NTBs have been adapted during the pandemic with the increased use of virtual technology. Virtual NTBs were found to be beneficial, yet administrative support is lacking in some places.ConclusionsVirtual implementation of NTBs was feasible and accepted in the centers surveyed. Therefore, successful implementation offers new avenues and may be pursued for networking between centers, thereby increasing coverage of neuro-oncology care.

Protein SUMOylation is a dynamic post-translational modification shown to be involved in a diverse set of physiologic processes throughout the cell. SUMOylation has also been shown to play a role in the pathobiology of myriad cancers, one of which is glioblastoma multiforme (GBM). As such, the clinical significance and therapeutic utility offered via the selective control of global SUMOylation is readily apparent. There are, however, relatively few known/effective inhibitors of global SUMO-conjugation. Herein we describe the identification of topotecan as a novel inhibitor of global SUMOylation. We also provide evidence that inhibition of SUMOylation by topotecan is associated with reduced levels of CDK6 and HIF-1α, as well as pronounced changes in cell cycle progression and cellular metabolism, thereby highlighting its putative role as an adjuvant therapy in defined GBM patient populations.

Background: Hydrogen peroxide (H2O2) is a well-known hemostatic and antiseptic agent in neurosurgical practice. While there are concerns regarding the use of H2O2 due to its potential for neuronal damage, the pathophysiological effect on neuronal cells is not clearly understood. Methods: An online survey concerning the use of H2O2 was conducted in a board-certified platform, and an experimental study was designed to investigate the effect of H2O2 on neuronal and tumor cells. Brain tissues of mice and brain/tumor tissues of humans were irrigated with H2O2 3%, H2O2 1.5%, and NaCl 0.9%, and processed by bipolar coagulation. Tissue sections were obtained and stained with H&E and analyzed by the depth and degree of neuronal damage measured from the cortical surface (μm). Results: In total, 242 neurosurgeons participated in the survey, and 81% of neurosurgeons reported use of H2O2 in neurosurgical practice. however only 5% of the participants had a literature-based knowledge of the pathophysiological mechanism of H2O2. In total, eight mouse brain tissues, 21 human brain tissues, and seven human tumor tissues were processed and analyzed. The experimental study found that H2O2 caused vacuolization of neuronal tissue in mouse brain tissues, with a mean depth of damage of 343.7 ± 39.7 μm after 2 min and 460.1 ± 36.4 μm after 10 min exposure to H2O2 3% (p < 0.001). In human brain tissues, vacuolization was detected in sections exposed to H2O2 1.5% and 3%, with a mean depth of damage of 543.8 ± 304.5 μm and 859.0 ± 379 μm (p = 0.003). In the bipolar coagulation group, the mean depth of neuronal damage, of 2504 ± 1490 μm, was nearly three times greater than that in the H2O2 group (p < 0.001). Similar results were observed in human tumor tissues as well. Conclusions: H2O2 seems to cause less local damage on neuronal and tumor cells than conventional bipolar cauterization, suggesting it as a good alternative to be used for hemostasis and marginal tumor cell treatment. However, due to its potential risk for embolism, H2O2 should be used with caution.

The small, ubiquitin-like modifier (SUMO) is a post-translational modifier with a profound influence on several key biological processes, including the mammalian stress response. Of particular interest are its neuroprotective effects, first recognized in the 13-lined ground squirrel (Ictidomys tridecemlineatus), in the context of hibernation torpor. Although the full scope of the SUMO pathway is yet to be elucidated, observations of its importance in managing neuronal responses to ischemia, maintaining ion gradients, and the preconditioning of neural stem cells make it a promising therapeutic target for acute cerebral ischemia. Recent advances in high-throughput screening have enabled the identification of small molecules that can upregulate SUMOylation, some of which have been validated in pertinent preclinical models of cerebral ischemia. Accordingly, the present review aims to summarize current knowledge and highlight the translational potential of the SUMOylation pathway in brain ischemia.