Xenon anesthesia for awake craniotomy: safety and efficacy.

BACKGROUND: The asleep-awake-asleep (AAA) craniotomy is a technique that offers the opportunity of having a patient fully cooperative during the awake phase, and minimizes the possible discomfort, due to the asleep phase. The aim of this prospective observational study was to test the use of xenon in the first asleep phase of an AAA craniotomy, in patients undergoing craniotomy for brain tumor resection. METHODS: The data have been collected from 40 awake craniotomy procedures, performed in patients with cerebral tumor, treated with the AAA technique. Patients were treated with xenon during the asleep phase, and quality of mapping, complications and qualitative judgment of the experience given by the patients were recorded. RESULTS: The mapping was carried out as planned in 37 out of 40 cases. The doses of xenon administered during the first asleep phase of the anesthesia was 13±2 L. Time for awakening after xenon was switched off was 5±1 minute. A combination of xenon and regional anesthesia (with no need for additional systemic anesthetics) was adequate to accomplish craniotomy in 27/40 patients (67.5%). On the day after the operation, 37 patients recalled the testing procedure for mapping during the awake period, none had recollection of local anesthetic injections for regional anesthesia or sound associated with the neurosurgical drill. Five patients (12.5%) reported mild pain during tumor removal (VAS Score less than three). CONCLUSIONS: In this case series, xenon anesthesia was successfully used for the sedative phase of an awake craniotomy accomplished with an AAA approach.

A phase II, randomized, study of weekly APG101+reirradiation versus reirradiation in progressive glioblastoma.

PURPOSE: Preclinical data indicate anti-invasive activity of APG101, a CD95 ligand (CD95L)-binding fusion protein, in glioblastoma. EXPERIMENTAL DESIGN: Patients (N = 91) with glioblastoma at first or second progression were randomized 1:2 between second radiotherapy (rRT; 36 Gy; five times 2 Gy per week) or rRT+APG101 (400 mg weekly i.v.). Patient characteristics [N = 84 (26 patients rRT, 58 patients rRT+APG101)] were balanced. RESULTS: Progression-free survival at 6 months (PFS-6) rates were 3.8% [95% confidence interval (CI), 0.1-19.6] for rRT and 20.7% (95% CI, 11.2-33.4) for rRT+APG101 (P = 0.048). Median PFS was 2.5 (95% CI, 2.3-3.8) months and 4.5 (95% CI, 3.7-5.4) months with a hazard ratio (HR) of 0.49 (95% CI, 0.27-0.88; P = 0.0162) adjusted for tumor size. Cox regression analysis adjusted for tumor size revealed a HR of 0.60 (95% CI, 0.36-1.01; P = 0.0559) for rRT+APG101 for death of any cause. Lower methylation levels at CpG2 in the CD95L promoter in the tumor conferred a stronger risk reduction (HR, 0.19; 95% CI, 0.06-0.58) for treatment with APG101, suggesting a potential biomarker. CONCLUSIONS: CD95 pathway inhibition in combination with rRT is an innovative concept with clinical efficacy. It warrants further clinical development. CD95L promoter methylation in the tumor may be developed as a biomarker.