LAUSR

Mutations in the KCNQ2 gene that encodes for a voltage‐dependent potassium channel subunit 7.2 (kv 7.2) are associated with a wide clinical spectrum ranging from milder variants such as benign familial neonatal seizures to a severe phenotype of neonatal‐onset developmental and epileptic encephalopathy (DEE).[1] The severe end of the spectrum, which is associated with either suppression burst pattern or multifocal epileptiform discharges on electroencephalography (EEG), is called KCNQ2 encephalopathy. It is not clear from the literature whether it is the type of genetic mutation or it is the recurrent clinical and sub‐clinical seizures before appropriate treatment is instituted that leads to the poor outcome.[2‐5] If the latter statement is true, then early institution of appropriate anti‐seizure medications in the form of sodium channel blockers (SCBs) can result in quick and good seizure control, thereby improving the neurodevelopmental outcome.