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Neonatal onset epilepsies are infrequent compared with neonatal seizures caused by acute symptomatic etiologies. Etiologies of neonatal epilepsies are classified into structural, genetic, and metabolic causes. EEG and amplitude-integrated EEG (aEEG) are essential for the diagnosis and monitoring of these conditions. EEG/aEEG findings often differ substantially among infants; unusual findings, such as downward seizure patterns on aEEG, can be found. Focal-onset seizures are very frequent, and epileptic spasms are infrequently observed. Myoclonic seizures with ictal EEG correlates and generalized tonic seizures are exceptional. Although burst suppression is known as the EEG hallmark of early infantile epileptic encephalopathy (EIEE) and early myoclonic encephalopathy (EME), the definition of “burst suppression” differs among researchers. Additional information is necessary to better understand the EEG/aEEG findings related to neonatal epilepsies and to clarify their utility in the diagnosis of neonatal epilepsies and monitoring the efficacy of treatment.
Benign familial neonatal seizures (BFNS) are concerned with a familial history of benign neonatal seizures (BNS). Basic mechanisms in this syndrome are probably close to those involved in other types of neonatal convulsions. The immature brain is more likely to respond to any kind of injury with epileptic seizures. If recordings are made, the electroclinical presentation of seizures is relatively stereotyped. Computed tomography (CT) or magnetic resonance imaging (MRI) is not indicated as long as the neurological state of the baby remains normal. In experience, sodium valproate was effective, leading to rapid cessation of seizures. Recognizing the phenotype of BFNS is important, first because of the prediction of a favorable neurological outcome, and second for the contribution to genetic studies, which comprise a dynamic area of epilepsy research, not only for the idiopathic epilepsies but also for the development of new antiepileptic drugs.
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