Neonatal seizures are a common problem inadequately treated with standard GABAergic anticonvulsants. Understanding how the ontogeny of neuronal cation/chloride cotransporter expression renders GABAergic signaling excitatory in the neonatal brain has helped explain the increased seizure propensity and poor efficacy of GABAergic anticonvulsants in newborns, has provided insight into the mechanism of electroclinical uncoupling, and has served as the rationale underlying the proposed polypharmaceutical approach of treating neonatal seizures with bumetanide and phenobarbital that is currently being investigated in two large international trials.
Copyright © 2012, Michael A Rogawski, Antonio V Delgado-Escueta, Jeffrey L Noebels, Massimo Avoli and Richard W Olsen.