Vagal nerve stimulation is an important adjunctive therapy for medically refractory epilepsy and major depression. Additionally, it may prove effective in treating obesity, Alzheimer's disease, and some neuropsychiatic disorders. As the number of approved indications increases, more patients are becoming eligible for surgical placement of a commercial vagal nerve stimulator (VNS). Initial VNS placement typically requires general anesthesia, and patients with previously implanted devices may present for other surgical procedures requiring anesthetic management. In this review, we will focus on the indications for vagal nerve stimulation (both approved and experimental), proposed therapeutic mechanisms for vagal nerve stimulation, and potential perioperative complications during initial VNS placement. Anesthetic considerations during initial device placement, as well as anesthetic management issues for patients with a preexisting VNS, are reviewed.

IDH1 mutations in gliomas associate with longer survival. Prooxidant and antiproliferative effects of IDH1 mutations and its D-2-hydroxyglutarate (2-HG) product have been described in vitro, but inconsistently observed. It is also unclear whether overexpression of mutant IDH1 in wild-type cells accurately phenocopies the effects of endogenous IDH1-mutations on tumor apoptosis and autophagy. Herein we investigated the effects of 2-HG and mutant IDH1 overexpression on proliferation, apoptosis, oxidative stress, and autophagy in IDH1 wild-type glioma cells, and compared those results with patient-derived tumors. 2-HG reduced viability and proliferation of U87MG and LN18 cells, triggered apoptosis in LN18 cells, and autophagy in U87MG cells. In vitro studies and flank xenografts of U87MG cells overexpressing R132H IDH1 exhibited increased oxidative stress, including increases of both manganese superoxide dismutase (MnSOD) and p62. Patient-derived IDH1-mutant tumors showed no significant differences in apoptosis or autophagy, but showed p62 accumulation and actually trended toward reduced MnSOD expression. These data indicate that mutant IDH1 and 2-HG can induce oxidative stress, autophagy, and apoptosis, but these effects vary greatly according to cell type.

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A neural network was developed that utilizes both clinical and imaging (CT and MRI) data to predict posterior fossa tumor (PFT) type. Data from 33 children with PFTs were used to develop and test the system. When all desired information was available, the network was able to correctly classify 85.7% of the tumors. In cases with incomplete data, it was able to correctly classify 72.7% of the tumors. In both instances, the diagnoses made by the network were more likely to be correct than those made by the neuroradiologists.

We reviewed the records of the 957 shunt-related operations performed at Cardinal Glennon Children’s Hospital over a 10-year period. During that time, 94 shunt infections were recognized. Eight of the infections occurred more than 9 months postoperatively. These differed from early infections in two ways: (1) Staphylococcus aureus was not found to be a pathogen in any late infection. (2) Abdominal pseudocysts were much more frequently found in patients with late-developing infections. In addition, the pathogens involved and the temporal distribution of cases suggest most infections that occur more than 9 months postoperatively are more likely caused by secondary bacterial seeding than by bacterial inoculation at the time of operation.