Accuracy of Depth Electrodes is Not Time-Dependent in Robot-Assisted Stereoelectroencephalography in a Pediatric Population.

BACKGROUND AND OBJECTIVES: Robot-assisted stereoelectroencephalography (sEEG) is steadily supplanting traditional frameless and frame-based modalities for minimally invasive depth electrode placement in epilepsy workup. Accuracy rates similar to gold-standard frame-based techniques have been achieved, with improved operative efficiency. Limitations in cranial fixation and placement of trajectories in pediatric patients are believed to contribute to a time-dependent accumulation of stereotactic error. Thus, we aim to study the impact of time as a marker of cumulative stereotactic error during robotic sEEG. METHODS: All patients between October 2018 and June 2022 who underwent robotic sEEG were included. Radial errors at entry and target points as well as depth and Euclidean distance errors were collected for each electrode, excluding those with errors over 10 mm. Target point errors were standardized by planned trajectory length. ANOVA and error rates over time were analyzed using GraphPad Prism 9. RESULTS: Forty-four patients met inclusion criteria for a total of 539 trajectories. Number of electrodes placed ranged from 6 to 22. Average root mean squared error was 0.45 ± 0.12 mm. Average entry, target, depth, and Euclidean distance errors were 1.12 ± 0.41 mm, 1.46 ± 0.44 mm, -1.06 ± 1.43 mm, and 3.01 ± 0.71 mm, respectively. There was no significant increased error with each sequential electrode placed (entry error P -value = .54, target error P -value = .13, depth error P -value = .22, Euclidean distance P -value = .27). CONCLUSION: No decremental accuracy over time was observed. This may be secondary to our workflow which prioritizes oblique and longer trajectories first and then into less error-prone trajectories. Further study on the effect of level of training may reveal a novel difference in error rates.

Loss of survivin in the prostate epithelium impedes carcinogenesis in a mouse model of prostate adenocarcinoma.

The inhibitor of apoptosis protein survivin is expressed in most cancers. Using the conditional PTEN deletion mouse model, we previously reported that survivin levels increase with prostate tumor growth. Here we evaluated the functional role of survivin in prostate tumor growth. First, we demonstrated that mice lacking the survivin gene in prostate epithelium were fertile and had normal prostate growth and development. We then serially, from about 10-56 weeks of age, evaluated histopathologic changes in the prostate of mice with PTEN deletion combined with survivin mono- or bi-allelic gene deletion. While within this time period most of the animals with wild-type or monoallelic survivin deletion developed adenocarcinomas, the most severe lesions in the biallelic survivin deleted mice were high-grade prostatic intra-epithelial neoplasia with distinct histopathology. Many atypical cells contained large hypertrophic cytoplasm and desmoplastic reaction in the prostatic intra-epithelial neoplasia lesions of this group was minimal until the late ages. A reduced proliferation index as well as apoptotic and senescent cells were detected in the lesions of mice with compound PTEN/survivin deficiency throughout the time points examined. Survivin deletion was also associated with reduced tumor expression of another inhibitor of apoptosis member, the X-linked inhibitor of apoptosis. Our findings suggest that survivin participates in the progression of prostatic intraepithelial neoplasia to adenocarcinoma, and that survivin interference at the prostatic intraepithelial neoplasia stages may be a potential therapeutic strategy to halt or delay further progression.