Electrocorticography (ECoG) data are commonly obtained during drug-resistant epilepsy (DRE) workup, in which subdural grids and stereotaxic depth electrodes are placed on the cortex for weeks at a time, with the goal of elucidating seizure origination. ECoG data can also be recorded from neuromodulatory devices, such as responsive neurostimulation (RNS), which involves the placement of electrodes deep in the brain. Of the neuromodulatory devices, RNS is the first to use recorded ECoG data to direct the delivery of electrical stimulation in order to control seizures. In this review, we first introduced the clinical management for epilepsy, and discussed the steps from seizure onset to surgical intervention. We then reviewed studies discussing the emergence and therapeutic mechanism behind RNS, and discussed why RNS may be underperforming despite an improved seizure detection mechanism. We discussed the potential utility of incorporating machine learning techniques to improve seizure detection in RNS, and the necessity to change RNS targets for stimulation, in order to account for the network theory of epilepsy. We concluded by commenting on the current and future status of neuromodulation in managing epilepsy, and the role of predictive algorithms to improve outcomes.

Glioblastoma (GBM) is one of the most aggressive and devastating primary brain tumors, with a median survival of 15 months following diagnosis. Despite the intense treatment regimen which routinely includes maximal safe neurosurgical resection followed by adjuvant radio- and chemotherapy, the disease remains uniformly fatal. The poor prognosis associated with GBM is multifactorial owing to factors such as increased proliferation, angiogenesis, and metabolic switching to glycolytic pathways. Critically, GBM-mediated local and systemic immunosuppression result in inadequate immune surveillance and ultimately, tumor-immune escape. Microglia—the resident macrophages of the central nervous system (CNS)—play crucial roles in mediating the local immune response in the brain. Depending on the specific pathological cues, microglia are activated into either a pro-inflammatory, neurotoxic phenotype, known as M1, or an anti-inflammatory, regenerative phenotype, known as M2. In either case, microglia secrete corresponding pro- or anti-inflammatory cytokines and chemokines that either promote or hinder tumor growth. Herein, we review the interplay between GBM cells and resident microglia with a focus on contemporary studies highlighting the effect of GBM on the subtypes of microglia expressed, the associated cytokines/chemokines secreted, and ultimately, their impact on tumor pathogenesis. Finally, we explore how understanding the intricacies of the tumor-immune landscape can inform novel immunotherapeutic strategies against this devastating disease.