A treatment paradigm for neonatal seizures based on the ontogeny of neuronal chloride/cation cotransporter expression in the human cortex

作者：Kahle Kristopher T; Staley Kevin J^*

来源：Epilepsia, 2010, 51: 89-89.

DOI：10.1111/j.1528-1167.2010.02875.x

• Bumetanide
• Chloride concentration
• Epilepsy
• GABA(A) receptors
• NKCC1
• Neonatal seizures
• Reversal potential

P>Neonatal seizures are a common problem inadequately treated with standard gamma-aminobutyric acid (GABA)ergic 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, and is the rational underlying the polypharmaceutical approach to treating neonatal seizures with bumetanide and phenobarbital. For an expanded treatment of this topic see Jasper's basic mechanisms of the epilepsies. 4th ed. (Noebels JL, Avoli M, Rogawski MA, Olsen RW, Delgado-Escueta AV, eds) published by Oxford University Press (available on the National Library of Medicine Bookshelf [NCBI] at http://www.ncbi.nlm.nih.gov/books).

• 出版日期2010-12