Background: Presurgical three-dimensional (3D) reconstructions allow spatial localization of cerebral lesions and their relationship with adjacent anatomical structures for optimal surgical resolution. The purpose of the present article is to present a method of virtual preoperative planning aiming to enhance 3D comprehension of neurosurgical pathologies using free DICOM image viewers. Case Description: We describe the virtual presurgical planning of a 61-year-old female presenting a cerebral tumor. 3D reconstructions were created with the “Horos^®” Digital Imaging and Communications in Medicine viewer, utilizing images obtained from contrast-enhanced brain magnetic resonance imaging and computed tomography. The tumor and adjacent relevant structures were identified and delimited. A sequential virtual simulation of the surgical stages for the approach was performed with the identification of local gyral and vascular patterns of the cerebral surface for posterior intraoperative recognition. Through virtual simulation, an optimal approach was gained. Accurate localization and complete removal of the lesion were achieved during the surgical procedure. Virtual presurgical planning with open-source software can be utilized for supratentorial pathologies in both urgent and elective cases. Virtual recognition of vascular and cerebral gyral patterns is helpful reference points for intraoperative localization of lesions lacking cortical expression, allowing less invasive corticotomies. Conclusion: Digital manipulation of cerebral structures can increase anatomical comprehension of neurosurgical lesions to be treated. 3D interpretation of neurosurgical pathologies and adjacent anatomical structures is essential for developing an effective and safe surgical approach. The described technique is a feasible and accessible option for presurgical planning.

The close interaction between neurons and astrocytes has been extensively studied. However, the specific behavior of these cells after ischemia-reperfusion injury and hypothermia remains poorly characterized. A growing body of evidence suggests that mitochondria function and putative transference between neurons and astrocytes may play a fundamental role in adaptive and homeostatic responses after systemic insults such as cardiac arrest, which highlights the importance of a better understanding of how neurons and astrocytes behave individually in these settings. Brain injury is one of the most important challenges in post-cardiac arrest syndrome, and therapeutic hypothermia remains the single, gold standard treatment for neuroprotection after cardiac arrest. In our study, we modeled ischemia-reperfusion injury by using in vitro enhanced oxygen-glucose deprivation and reperfusion (eOGD-R) and subsequent hypothermia (HPT) (31.5 °C) to cell lines of neurons (HT-22) and astrocytes (C8-D1A) with/without hypothermia. Using cell lysis (LDH; lactate dehydrogenase) as a measure of membrane integrity and cell viability, we found that neurons were more susceptible to eOGD-R when compared with astrocytes. However, they benefited significantly from HPT, while the HPT effect after eOGD-R on astrocytes was negligible. Similarly, eOGD-R caused a more significant reduction in adenosine triphosphate (ATP) in neurons than astrocytes, and the ATP-enhancing effects from HPT were more prominent in neurons than astrocytes. In both neurons and astrocytes, measurement of reactive oxygen species (ROS) revealed higher ROS output following eOGD-R, with a non-significant trend of differential reduction observed in neurons. HPT after eOGD-R effectively downregulated ROS in both cells; however, the effect was significantly more effective in neurons. Lipid peroxidation was higher after eOGD-R in neurons, while in astrocytes, the increase was not statistically significant. Interestingly, HPT had similar effects on the reduction in lipoperoxidation after eOGD-R with both types of cells. While glutathione (GSH) levels were downregulated after eOGD-R in both cells, HPT enhanced GSH in astrocytes, but worsened GSH in neurons. In conclusion, neuron and astrocyte cultures respond differently to eOGD-R and eOGD-R + HTP treatments. Neurons showed higher sensitivity to ischemia-reperfusion insults than astrocytes; however, they benefited more from HPT therapy. These data suggest that given the differential effects from HPT in neurons and astrocytes, future therapeutic developments could potentially enhance HPT outcomes by means of neuronal and astrocytic targeted therapies.