Neonatal Seizures: Diagnosis, Etiologies, and Management

Julie Ziobro, MD, PhD; Renée A. Shellhaas, MD, MS

Disclosures

Semin Neurol. 2020;40(2):246-256. 

In This Article

Outcomes

Early-life seizures contribute to the pathological enhancement of synaptic connections in the hippocampus in the period following ictal activity. This alters normal synaptogenesis and may contribute to later cognitive deficits.[9,71] Seizures impair synapse proliferation and synaptic plasticity, and may affect ion channel and synapse function, myelination, dendritic branching, and overall brain development.[5,9,71–74] As a result, animal models of recurrent early-life seizures demonstrate long-term functional, morphological, and physiologic deficits.[74,75]

Despite advances in neonatal intensive care, in-hospital mortality remains high for newborns with seizures (35% mortality for preterms and 15% for term infants in one recent consecutive cohort).[21] The risks for long-term adverse neurologic sequelae have also remained stable. Approximately 30% of infants who survive neonatal seizures suffer from long-term neurologic impairments, such as cerebral palsy, intellectual disabilities, and postneonatal epilepsy.[4] Longer duration of EEG seizures has been associated with increased risk of mortality and morbidity,[76] while increased seizure severity has been linked to worse injury on brain MRI. Additionally, at the age of 4 years, children who had a higher neonatal seizure severity score had more motor and cognitive impairment than those with lower seizure burden, and this effect was independent of neonatal MRI abnormalities. These data suggest that neonatal seizures may induce neuronal injury or exacerbate existing brain injuries.[76]

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