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1.
World Neurosurg ; 182: e486-e492, 2024 Feb.
Article in English | MEDLINE | ID: mdl-38042289

ABSTRACT

BACKGROUND: Stereoelectroencephalography (SEEG) remains critical in guiding epilepsy surgery. Robot-assisted techniques have shown promise in improving SEEG implantation outcomes but have not been directly compared. In this single-institution series, we compared ROSA and Stealth AutoGuide robots in pediatric SEEG implantation. METHODS: We retrospectively reviewed 21 sequential pediatric SEEG implantations consisting of 6 ROSA and 15 AutoGuide procedures. We determined mean operative time, time per electrode, root mean square (RMS) registration error, and surgical complications. Three-dimensional radial distances were calculated between each electrode's measured entry and target points with respective errors from the planned trajectory line. RESULTS: Mean overall/per electrode operating time was 73.5/7.5 minutes for ROSA and 126.1/10.9 minutes for AutoGuide (P = 0.030 overall, P = 0.082 per electrode). Mean RMS registration error was 0.77 mm (0.55-0.93 mm) for ROSA and 0.6 mm (0.2-1.0 mm) for AutoGuide (P = 0.26). No procedures experienced complications. The mean radial (entry point error was 1.23 ± 0.11 mm for ROSA and 2.65 ± 0.12 mm for AutoGuide (P < 0.001), while the mean radial target point error was 1.86 ± 0.15 mm for ROSA and 3.25 ± 0.16 mm for AutoGuide (P < 0.001). CONCLUSIONS: Overall operative time was greater for AutoGuide procedures, although there was no statistically significant difference in time per electrode. Both systems are highly accurate with no significant RMS error difference. While the ROSA robot yielded significantly lower entry and target point errors, both robots are safe and reliable for deep electrode insertion in pediatric epilepsy.


Subject(s)
Drug Resistant Epilepsy , Epilepsy , Robotic Surgical Procedures , Child , Humans , Robotic Surgical Procedures/methods , Retrospective Studies , Electroencephalography/methods , Stereotaxic Techniques , Epilepsy/surgery , Electrodes, Implanted , Drug Resistant Epilepsy/surgery
2.
Surg Neurol Int ; 13: 585, 2022.
Article in English | MEDLINE | ID: mdl-36600777

ABSTRACT

Background: Medically refractory epilepsy constitutes up to one-third of the epilepsy pediatric patients. Corpus callosotomy (CC) has been used for the treatment of medically refractory epilepsy in children with atonic seizures and generalized tonic-clonic (GTC) seizures. In this case series study, we are describing a novel technique for CC using the frameless navigation probe through a minicraniotomy. Methods: Thirteen pediatric patients with the diagnosis of medically refractory epilepsy predominantly GTC with drop attack who underwent extensive Phase I. An L-shape was done, then through a 4 × 3 cm craniotomy, we were able to open the interhemispheric fissure until the corpus callosum is visualized. The Stealth probe is then used to go down to the midline raphe which is followed anteriorly then traced posteriorly to the anterior border of the vein of Galen. Finally, the Stealth probe is used to confirm the completeness of the callosotomy. Results: The procedure was accomplished successfully with no intraoperative complications; mean surgical time is 3 h:07 m. The mean follow-up was 31.5 months. All patients achieved significant seizure control. No patients experienced worsening of their atonic seizures after surgery compared with their preoperative state; however, six patients achieved Engel Class I, four patients achieved Engel Class II, and three patients achieved Engel Class III. Conclusion: Complete CC using a frameless navigation probe is a novel and effective technique for the treatment of medically refractory epilepsy with a very good surgical and seizure outcomes, minimal neurological morbidity, minimal blood loss, and short OR time.

3.
Radiat Res ; 177(6): 751-65, 2012 Jun.
Article in English | MEDLINE | ID: mdl-22559204

ABSTRACT

Radiation-induced bystander effects have been extensively studied at low doses, since evidence of bystander induced cell killing and other effects on unirradiated cells were found to be predominant at doses up to 0.5 Gy. Therefore, few studies have examined bystander effects induced by exposure to higher doses of radiation, such as spatially fractionated radiation (GRID) treatment. In the present study, we evaluate the ability of GRID treatment to induce changes in GRID adjacent (bystander) regions, in two different murine carcinoma cell lines following exposure to a single irradiation dose of 10 Gy. Murine SCK mammary carcinoma cells and SCCVII squamous carcinoma cells were irradiated using a brass collimator to create a GRID pattern of nine circular fields 12 mm in diameter with a center-to-center distance of 18 mm. Similar to the typical clinical implementation of GRID, this is approximately a 50:50 ratio of direct and bystander exposure. We also performed experiments by irradiating separate cultures and transferring the medium to unirradiated bystander cultures. Clonogenic survival was evaluated in both cell lines to determine the occurrence of radiation-induced bystander effects. For the purpose of our study, we have defined bystander cells as GRID adjacent cells that received approximately 1 Gy scatter dose or unirradiated cells receiving conditioned medium from irradiated cells. We observed significant bystander killing of cells adjacent to the GRID irradiated regions compared to sham treated controls. We also observed bystander killing of SCK and SCCVII cells cultured in conditioned medium obtained from cells irradiated with 10 Gy. Therefore, our results confirm the occurrence of bystander effects following exposure to a high-dose of radiation and suggest that cell-to-cell contact is not required for these effects. In addition, the gene expression profile for DNA damage and cellular stress response signaling in SCCVII cells after GRID exposure was studied. The occurrence of GRID-induced bystander gene expression changes in significant numbers of DNA damage and cellular stress response signaling genes, providing molecular evidence for possible mechanisms of bystander cell killing.


Subject(s)
Bystander Effect/radiation effects , Carcinoma, Squamous Cell/genetics , Carcinoma, Squamous Cell/pathology , Dose Fractionation, Radiation , Gene Expression Regulation, Neoplastic/radiation effects , Mammary Neoplasms, Experimental/genetics , Mammary Neoplasms, Experimental/pathology , Animals , Bystander Effect/genetics , Cell Line, Tumor , Cell Survival/radiation effects , DNA Damage , Dose-Response Relationship, Radiation , Film Dosimetry , Mice , Oxidative Stress/radiation effects , Signal Transduction/radiation effects
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