BackgroundTumors with cysts often correlate with gliomas, metastatic tumors, or hemangioblastomas, which require differentiation.MethodsThirty-eight cases of cyst associated-meningioma based on preoperative radiologic studies and histologic confirmations were reviewed from November 1998 to July 2017.ResultsA total of 395 cases of meningioma were observed in the 20 years, and surgical treatment of intracranial meningioma was performed in 120 cases. Thirty-eight (9.6%) cases of cyst associated meningiomas were analyzed. Nauta type I was the most common type of cyst (39.5%) and the most frequent histopathological subtype was meningothelial type (36.8%).ConclusionStatistically there were no significant associations between meningioma histopathological type and associated cysts; however, the rate of World Health Organization grade II was higher in cyst associated meningiomas than in unrelated meningiomas. This correlation was weak, in accordance with the meningioma grade.
Background/Aim: Poly (ADP-ribose) polymerase (PARP) inhibition could enhance the efficacy of temozolomide and prolong survival in patients with glioblastoma. The aim of this study was to evaluate the combination of the PARP inhibitor olaparib with temozolomide in the treatment of glioblastoma. Materials and Methods: The in vitro and in vivo antitumor effects of the PARP inhibitor olaparib together with temozolomide were evaluated. The in vitro experimental glioblastoma model involved O 6 -methylguanine methyltransferase (MGMT) promoter-methylated (U87MG, U251MG) and MGMT promoter-unmethylated (T98G) glioblastoma cell lines using In this model cell viability and apoptosis were assessed. For the in vivo studies, nude mice bearing orthotopically xenografted glioblastoma cell lines (U87MG) were randomized to four experimental groups: i) the untreated, ii) temozolomide alone, iii) olaparib alone and iv) olaparib and temozolomide combination groups. Mice were treated daily for 4 weeks and monitored for tumor growth and survival. Results: In vitro we found that the combination of olaparib with temozolomide enhanced temozolomideinduced cytotoxicity in all glioblastoma cell lines regardless of the status of MGMT promoter methylation. In vivo, mice treated with temozolomide alone or in combination with olaparib showed greater survival than those untreated or with the olaparib monotherapy, as well as significantly decreased tumor volume. There was no significant difference in survival and tumor volume between temozolomide alone and the combination treatment. Conclusion: The combination of the PARP inhibitor olaparib with temozolomide could be promising candidates for combination therapy of glioblastoma regardless of the MGMT promoter methylation status.Glioblastoma is the most common and deadliest glioma subtype in adults, with an age-adjusted incidence of 0.59 to 3.69 per 100,000 persons (1). Glioblastoma has a highly aggressive behavior, and, without any treatment, its median overall survival (OS) is limited to approximately 3 to 6 months. The standard care includes maximal safe resection, followed by concurrent chemoradiotherapy with temozolomide (TMZ) and subsequent treatment with adjuvant temozolomide, which is named Stupp's protocol (2).Although patients with glioblastoma are treated multimodally, the prognosis remains poor. The median OS is still limited to 14.6 months, while the OS rate after 2 years is 27%, dropping down to 3% to 7% after 5 years (2, 3). Additionally, almost all glioblastoma patients' relapse, and over 86% of their recurrences are in the irradiation field (4). The difficulty of treating glioblastoma is due to several complicating factors. As glioblastoma is a brain tumor, treatments are restricted by the blood-brain barrier (BBB) and by the risks it bears due to the uniqueness of the brain tissue, profound susceptibility to interstitial chemotherapy and limited repair capacity (5). In addition, glioblastoma cells are considered chemo-and radioresistant (2, 6, 7).The resistance to treatment could be...
Background: No dural substitute has proven to be complication-free in a large clinical trial, even suggesting some benefit during watertight closure. However, primary dural closure is not always possible due to dural shrinkage from electrocautery for dural bleeding. Objective: This study is performed to analyze the clinical outcomes related to cerebrospinal fluid (CSF) leakage after microvascular decompression (MVD) using a simple surgical technique. Methods: Three hundred and sixty consecutive cases were treated with MVD and followed up for more than one month after surgery. Bleeding from the cut veins during dural incision was controlled by pulling stay sutures instead of electrocautery to avoid dural shrinkage. Additionally, a wet cottonoid was placed on the cerebellar side dural flap to prevent dural dehydration. During dural closure, primary dural closure was always attempted. If not possible, a “plugging muscle” method was used for watertight dural closure. Results: The mean age was 54.1 ± 10.8 years (range, 24–85 years), and 238 (66.1%) were female. Primary MVD was performed in 345 (95.8%) patients. The mean operation time (from skin incision to skin closure) was 96.7 ± 33.0 min (range, 38–301 min). Primary dural closure was possible in 344 (95.6%) patients. The “plugging muscle method” was performed more frequently in patients older than 60 years (8 of 99 cases, 8.08%) than in younger cases (8 of 261 cases, 3.07%) (p = 0.039; chi-squared test). After surgery, 5 (1.4%) patients were treated for middle ear effusion, and another 5 (1.4%) patients experienced transient CSF rhinorrhea, which was spontaneously resolved within 1 to 7 days. No patients required additional treatments for CSF leakage. Conclusion: A simple technique using pulling stay sutures to stop bleeding from the dural edges and placing a wet cottonoid on the exposed dura can make primary dural closure easier.
Background High-grade glioma (HGG) with primary leptomeningeal seeding (PLS) at initial diagnosis is rare. The purpose of this study was to identify its clinical features and to describe the clinical treatment outcomes. Methods We retrospectively reviewed the medical records of patients with HGG (World Health Organization grade III or IV) at our institution between 2004 and 2019, and patients with PLS at the initial diagnosis were enrolled in the study. Clinical features, such as the location of leptomeningeal seeding, surgical methods, and degree of resection, were sorted based on electronic medical records also containing performance scale, and hematological and serological evaluations. Radiological findings and immunohistochemical categories were confirmed. Furthermore, we sought to determine whether controlling intracranial pressure (ICP) via early cerebrospinal fluid (CSF) diversion increases overall survival (OS) after the initial diagnosis. Results Of the 469 patients with HGG in our institution, less than 2% had PLS at the initial diagnosis. Most patients suffered from headache, diplopia, and dizziness. Pathological findings included 7 glioblastomas and 2 anaplastic astrocytomas. Seven of the 9 patients underwent CSF diversion. All patients were administered concurrent chemoradiotherapy (CCRT) with temozolomide, 89% of which started adjuvant temozolomide and 33% of which completed the six cycles of adjuvant temozolomide. The OS of patients with HGG and PLS was 8.7 months (range, 4-37), an extremely poor result compared to that of other studies. Also, the 1-year and 2-year OS rates were 44.4% and 16.7%, respectively. Conclusion Diagnosis and treatment of HGG with PLS are challenging. Aggressive control of ICP followed by early initiation of standard CCRT seems to be helpful in improving symptoms. However, despite aggressive treatment, the prognosis is poor. A multicenter trial and research may be necessary to create a standardized protocol for this disease.
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