Oxidative stress is known to induce cell death in a wide variety of cell types, apparently by modulating intracellular signaling pathways. Activation of extracellular signal-regulated kinase (ERK) in oxidative stress remains controversial. In some cellular systems, the ERK activation is associated with protection against oxidative stress, while in other system, the ERK activation is involved in apoptotic cell death. The present study was undertaken to examine the role of ERK activation in H2O2-induced cell death of human glioma (A172) cells. H2O2 resulted in a time- and dose-dependent cell death, which was largely attributed to apoptosis. H2O2 treatment caused marked sustained activation of ERK. The ERK activation and cell death induced by H2O2 was prevented by catalase, the hydrogen peroxide scavenger, and U0126, an inhibitor of ERK upstream kinase MEK1/2. Transient transfection with constitutive active MEK1, an upstream activator of ERK1/2, increased H2O2-induced cell death, whereas transfection with dominant-negative mutants of MEK1 decreased the cell death. The ERK activation and cell death caused by H2O2 was inhibited by antioxidants (N-acetylcysteine and trolox), Ras inhibitor, and suramin. H2O2 produced depolarization of mitochondrial membrane potential and its effect was prevented by catalase and U0126. Taken together, these findings suggest that growth factor receptor/Ras/MEK/ERK signaling pathway plays an active role in mediating H2O2-induced apoptosis of human glioma cells and functions upstream of mitochondria-dependent pathway to initiate the apoptotic signal.
The incidence and risk factors of symptomatic and asymptomatic hyponatremia were investigated in 94 patients who underwent transsphenoidal surgery and serum sodium level monitoring between January 2002 and December 2006. The records were retrospectively reviewed to determine the incidence and risk factors (age and sex, tumor size, endocrinologic findings) of hyponatremia. Postoperatively, the serum sodium levels of the patients were measured at least once within 2 or 3 days. Hyponatremia was found in 17 of the 94 patients, of whom 7 became symptomatic. The mean sodium level of symptomatic patients with hyponatremia at diagnosis was 123.5 mEq/l, compared with 129.8 mEq/l of asymptomatic patients. The serum sodium levels began to fall on mean postoperative day 7 and reached nadir on mean day 8. All 17 patients with hyponatremia were treated with mild fluid restriction. Four symptomatic patients with severe hyponatremia were treated with 3% hypertonic saline infusion in addition to fluid restriction. One symptomatic patient with severe hyponatremia was treated with fluid restriction only. All patients recovered within 5 days of management. Sex, tumor type, and tumor size did not correlate with development of delayed hyponatremia, but patients aged AE50 years were more likely to develop hyponatremia. Postoperative hyponatremia after transsphenoidal surgery is more common than previously reported and may lead to fatal complications. Therefore, all patients should undergo serum electrolyte level monitoring regularly for at least 1 or 2 weeks after transsphenoidal surgery.
Objective : The purpose of this study is to evaluate the clinical characteristics and surgical outcome of cerebellopontine angle (CPA) epidermoids presenting with trigeminal neuralgia. Methods : Between 1996 and 2004, 10 patients with typical symptoms of trigeminal neuralgia were found to have cerebellopontine angle epidermoids and treated surgically at our hospital. We retrospectively analyzed the clinico-radiological records of the patients. Results : Total resection was done in 6 patients (60%). Surgical removal of tumor and microvascular decompression of the trigeminal nerve were performed simultaneously in one case. One patient died due to postoperative aseptic meningitis. The others showed total relief from pain. During follow-up, no patients experienced recurrence of their trigeminal neuralgia (TN). Conclusion :The clinical features of TN from CPA epidermoids are characterized by symptom onset at a younger age compared to TN from vascular causes. In addition to removal of the tumor, the possibility of vascular compression at the root entry zone of the trigeminal nerve should be kept in mind. If it exists, a microvascular decompression (MVD) should be performed. Recurrence of tumor is rare in both total and subtotal removal cases, but long-term follow-up is required.
Cerebrospinal fluid (CSF) diversion is an essential component of neurosurgical care, but the rates and significance of hemorrhage associated with external ventricular drainage (EVD) and ventriculoperitoneal (VP) shunt procedures have not been well quantified. In this retrospective study, the authors examined the frequencies of hemorrhagic complications associated with EVD and VP shunt procedures, and attempted to identify associated risk factors. The treatment records of 370 EVDs in 276 patients and 102 VP shunts in 96 patients performed between 2008 and 2010 were retrospectively reviewed. Post-insertion computed tomographic (CT) scans were analyzed for any new hemorrhage related to the ventricular catheter. The effects of diagnosis at admission, endovascular treatment, anti-platelet medication, and a concurrent craniotomy operation were included in the analysis conducted to identify risk factors of ventricular catheterrelated hemorrhage. Hemorrhage following EVD was detected on CT scans in 76 (20.5%) of the 370 cases. However, symptomatic hemorrhage occurred in only 5 cases (1.4% of all EVDs). VP shunt was associated with a higher incidence of ventricular catheter-related hemorrhage than EVD (hemorrhage rate: 43.1%) and the rate of detectable neurological change was 2.9%. Multivariate logistic-regression analysis of risk factors of EVD-related hemorrhage identified preoperative anti-platelet medication as the only significant factor (odds ratio, 3.583 [95% confidence interval, 1.353 to 9.486]; p = 0.010). Ventriculostomy-related hemorrhagic complications were more common than anticipated, especially for the VP shunt procedure. However, such hemorrhages are rarely large, rarely the cause of neurological deterioration, and rarely require surgical removal. Preoperative anti-platelet medication appears to affect EVD-related hemorrhage development.
Glioblastoma multiforme (GBM) is the most aggressive intracranial tumor and it commonly spreads by direct extension and infiltration into the adjacent brain tissue and along the white matter tract. The metastatic spread of GBM outside of the central nervous system (CNS) is rare. The possible mechanisms of extraneural metastasis of the GBM have been suggested. They include the lymphatic spread, the venous invasion and the direct invasion through dura and bone. We experienced a 46-year-old man who had extraneural metastasis of the GBM on his left neck. The patient was treated with surgery for 5 times, radiotherapy and chemotherapy. He had survived 6 years since first diagnosed. Although the exact mechanism of the extraneural metastasis is not well understood, this present case shows the possibility of extraneural metastasis of the GBM, especially in patients with long survival.
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