• Hadar Flor-Hirsch, Eli Heyman, Ayelet Livneh, Orit Reish, Nathan Watemberg, Ita Litmanovits, Anat Ben Sason Lilli, Dorit Lev, Tally Lerman Sagie, and Haim Bassan.
• Pediatric Neurology and Development Center, Assaf Harofe Medical Center, Zerifin,, Neonatolgy Unit, Assaf Harofe Medical Center, Zerifin, Sackler faculty of medicine, Tel Aviv University, Tel Aviv.
• Epileptic Disord. 2018 Oct 1; 20 (5): 440-446.

AbstractVoltage-gated sodium channel alpha subunit 2 (SCN2A) gene mutations are associated with neonatal seizures and a wide range of epilepsy syndromes. Previous reports suggest that traditional sodium channel blockers (SCBs) such as phenytoin, carbamazepine, and lamotrigine have a beneficial effect on SCN2A-related neonatal seizures, as they counteract the gain-of-function effect of mutated Nav1.2 channels. Additionally, SCBs are beneficial against other sodium and potassium channel-related neonatal seizures. There are, however, few reports describing the effect of the new SCB lacosamide against neonatal and infantile epileptic seizures. We report herein two neonates with intractable neonatal seizures with SCN2A pathogenic missense variants. Both infants showed temporary seizure relief following IV administrations of phenytoin, but were resistant to a combination of antiepileptic drugs, while complete seizure control was achieved following lacosamide administration. We suggest that SCBs, e.g. phenytoin, should be introduced early for refractory neonatal seizures of non-lesional and presumably genetic origin. If any beneficial response to a SCB is noted, this should prompt an initiation of additional SCBs. New clinical trials will provide data on the efficacy and safety of the new SCB lacosamide for genetic neonatal seizures and perhaps neonatal seizures in general.

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