This condition manifests in newborns as brief and frequent episodes of tonic-clonic seizures with asymptomatic periods in between.

[2] Characteristically, seizure activity spontaneously ends during infancy and does not affect childhood development.

[3] Additionally, BFNS increases lifetime susceptibility to seizures as approximately 14% of those afflicted go on to develop epilepsy later in life.

BFNS often presents in the first week of life with brief but frequent episodes of tonic-clonic seizures, outside of which a child is completely asymptomatic.

[2][3][4] During the tonic phase of these seizures, infants may stop breathing (apnea) and consequently appear blue (cyanosis) due to lack of oxygen.

However, the appearance of a “theta pointu alternant pattern” and/or non-specific abnormalities on EEG has been reported in several cases, although their relationship to BFNE has not been well delineated.

[2][3][4] With that said, several studies tracking the health of patients with BFNE into adulthood have reported consequent intellectual disability[3] and seizure disorders.

The first of these mutations, G310V, leads to a 50% reduction in whole-cell current compared to cells expressing wild-type channels.

This mutation leads to an approximately 40% reduction in whole-cell current compared to wild-type expressing cells.

[2] Recurrent seizures later in life are treated in the standard ways (covered in the main epilepsy article).

Depending on the severity, some infants are sent home with heart and oxygen monitors that are hooked to the child with stick on electrodes to signal any seizure activity.