This mounting observational data as to the deleterious effects of CSD has led to increased excitement regarding CSD as a novel target for prevention of delayed injury after diverse types of acute brain injury(16). The optimal target or agent has not been defined, but there are promising animal data supporting a wide variety of agents, primarily targeting NMDAVR, as this is thought to be an important factor in propagation of SD(17). Initial clinical case reports of the effect of ketamine being used as sedation in patients with severe TBI(18) led to a larger scale effort to retrospectively study the various anesthetics used for standard clinical care on the frequency of CSD in monitored patients(19). Using only the sedation medications for which there were >1000 cumulative hours of ECog recording while on that medication, the effects of propofol, fentanyl, midazolam, ketamine, morphine, and sufentanyl were examined. The study found a consistent effect of ketamine in decreased probability of CSD/h per patient. This was nearly linearly dose dependent, and importantly, in multivariate analysis, ketamine still emerged as having a significant effect on decreasing both occurrence of CSD as well as the occurrence of the more deleterious clusters of CSD(19).