The role of inflammation has been increasingly recognized in a wide range of neurological diseases, including epilepsy and status epilepticus.29-31 Neuroinflammation can impact network excitability in several ways, including activating microglia, reshaping synaptic input, and altering ion channel function. Thus, there is the potential to explore anti-inflammatory therapies for use in conjunction with conventional ASMs in the chronic therapy of epilepsies that are thought to be inflammatory in nature, such as Rasmussen encephalitis.32 In addition, the utility of some treatments for seizure categories not conventionally believed to be related to inflammatory mechanisms should be explored. This has the potential to perhaps reduce the refractory rate, or increase seizure control, for some groups of patients.