[Electroclinical recognition of SCN2A, SCN8A, KCNQ2, and KCNQ3 pathogenic variants].

Genetic epilepsies presenting in the neonatal period and early infancy require time-critical, mechanism-aware decisions. Amplitude-integrated EEG (aEEG) provides continuous bedside screening in the NICU, but its yield improves when seizures are confirmed and characterized with multichannel conventional EEG (referred to here as rEEG; the term "continuous EEG or cEEG" is reserved for prolonged monitoring). In KCNQ2/KCNQ3 and SCN2A channelopathies, a distinctive ictal aEEG sequence-brief initial attenuation/decrease, rapid rise, and postictal depression-correlates with reproducible ictal features on rEEG/cEEG. Recognizing this signature may prompt rapid genetic testing and, when clinically appropriate, earlier targeted therapy with sodium-channel blockers, reducing prolonged ineffective polytherapy. SCN8A shows broader electroclinical heterogeneity without a single signature; however, normal brain MRI combined with high early seizure burden (often bilateral tonic-clonic seizures) and a progressively abnormal EEG should raise suspicion. This narrative review provides a pragmatic framework for SCN2A, SCN8A, KCNQ2, and KCNQ3, integrates the phenotype spectrum (including self-limited forms with potentially normal EEG), highlights safety considerations (including SUDEP), and briefly summarizes emerging precision-therapy under clinical investigation.