Object Currently, the effectiveness of minimally invasive evacuation of intracerebral hemorrhage (ICH) utilizing the endoscopic method is uncertain and the technique is considered investigational. The authors analyzed their experience with this method in terms of case selection, surgical technique, and long-term results. Methods The authors performed a retrospective analysis of the clinical and radiographic data obtained in 68 patients treated with endoscope-assisted ICH evacuation. Rebleeding, morbidity, and mortality were recorded as primary end points. Hematoma evacuation rate was calculated by comparing the pre- and postoperative CT scans. Glasgow Coma Scale scores and scores on the extended Glasgow Outcome Scale (GOSE) were recorded at the 6-month postoperative follow-up. The technical aspect of this report explains details of the procedure, the instruments that are used, the methods for hemostasis, and the role of hemostatic agents in the management of intraoperative hemorrhage. The pertinent literature was reviewed and summarized. Results All surgeries were performed within 12 hours of ictus, and 84% of the surgeries were performed within 4 hours. The mortality rate was 5.9%, and surgery-related morbidity occurred in 3 cases (4.4%). The hematoma evacuation rate was 93% overall—96% in the putaminal group, 86% in the thalamic group, and 98% in the subcortical group. The rebleeding rate was 1.5%. The mean operative time was 85 minutes, and the average blood loss was 56 ml. The mean GOSE score was 4.9 at 6-month follow-up. The authors acknowledge the limitations of these preliminary results in a small number of patients. Conclusions The data suggest that early endoscope-assisted ICH evacuation is safe and effective in the management of supratentorial ICH. The rebleeding, morbidity, and mortality rates are low compared with rates reported in the literature for the traditional craniotomy method. This study also showed that early and complete evacuation of ICH may lead to improved outcomes in selected patients. However, the safety and efficacy of endoscope-assisted ICH evacuation should be further investigated in a large, prospective, randomized trial.

Although surgical excision of meningioma and its dural base is the most common primary management, skull base meningiomas are quite different, and contemporary management usually consists of multimodal treatment with the aim of achieving the best possible functional outcome and quality of life (QOL) for these patients. As surgery plays an important role in the treatment of skull base meningiomas, it is crucial for neurosurgeons to appreciate the surgical outcome and QOL after meningioma surgery. Outcome is usually measured for meningiomas in terms of morbidity, mortality, time to recurrence, and QOL. The extent of resection, tumor grade, proliferative markers, and tumor location are significant factors in predicting the surgical outcome. Therefore, we address each of these factors in detail in this review. Advances in recent decades in microsurgical techniques, neuroimaging modalities, neuroanesthesia, and perioperative intensive care have substantially improved the surgical outcome; therefore, most surgical outcomes discussed in this review are cited from contemporary literature (2000 to the present) in order to depict the surgical outcome of contemporary microsurgery.

BackgroundThe Cdc42-interacting protein-4, Trip10 (also known as CIP4), is a multi-domain adaptor protein involved in diverse cellular processes, which functions in a tissue-specific and cell lineage-specific manner. We previously found that Trip10 is highly expressed in estrogen receptor-expressing (ER+) breast cancer cells. Estrogen receptor depletion reduced Trip10 expression by progressively increasing DNA methylation. We hypothesized that Trip10 functions as a tumor suppressor and may be involved in the malignancy of ER-negative (ER-) breast cancer. To test this hypothesis and evaluate whether Trip10 is epigenetically regulated by DNA methylation in other cancers, we evaluated DNA methylation of Trip10 in liver cancer, brain tumor, ovarian cancer, and breast cancer.MethodsWe applied methylation-specific polymerase chain reaction and bisulfite sequencing to determine the DNA methylation of Trip10 in various cancer cell lines and tumor specimens. We also overexpressed Trip10 to observe its effect on colony formation and in vivo tumorigenesis.ResultsWe found that Trip10 is hypermethylated in brain tumor and breast cancer, but hypomethylated in liver cancer. Overexpressed Trip10 was associated with endogenous Cdc42 and huntingtin in IMR-32 brain tumor cells and CP70 ovarian cancer cells. However, overexpression of Trip10 promoted colony formation in IMR-32 cells and tumorigenesis in mice inoculated with IMR-32 cells, whereas overexpressed Trip10 substantially suppressed colony formation in CP70 cells and tumorigenesis in mice inoculated with CP70 cells.ConclusionsTrip10 regulates cancer cell growth and death in a cancer type-specific manner. Differential DNA methylation of Trip10 can either promote cell survival or cell death in a cell type-dependent manner.

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