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EEG changes during the perinatal period, infancy, childhood, and adolescence are concomitant with brain growth, myelination, expanding connectivity, and overall maturation, which are particularly fast during the first year of life. EEG aspects of early brain development are accessible in preterm during the third trimester of gestational age, and they evolve to full-term, infancy, and childhood EEG patterns. Each of these age periods shares specific EEG features that reach gross adult outlines in the first year. Interpreting EEG needs therefore a deep knowledge of pathological and normal EEG patterns with their variants belonging to each age range. Recording EEG during these periods also requires adapting the recording techniques to the specific age in order to obtain interpretable records. This chapter describes normal EEG features and variants, characteristic patterns of development, and some patterns that are unusual for age, from the neonatal period to adolescence.

Among nonsymptomatic epilepsies exhibiting several types of generalized seizures in children two syndromes were progressively identified: epilepsy with myoclonic-astatic seizures (MAE) and nonsymptomatic Lennox-Gastaut syndrome (LGS). Various approaches based on etiology, electroclinical semiology, and mathematical analysis have progressively helped to distinguish these two conditions. Both conditions preferentially affect boys. The course is stereotyped in MAE, characterized by progressive worsening of epilepsy, usual pharmacoresistance at onset and tonic-clonic seizures, myoclonus and frequent episodes of myoclonic status epilepticus. EEG shows 3Hz spike wave bursts characteristic of idiopathic generalized epilepsy together with slowing of the tracing. In LGS, major seizures are mainly atypical absences and tonic seizures with 0.5-2Hz slow spike-waves and eventually focal anomalies. Prognosis in both syndromes ranges from recovery without sequelae to pharmacoresistant epilepsy that has improved over the past 2 decades with the new generation antiepileptic compounds. Iatrogenic factors may contribute to the poor prognosis, mainly in MAE. Pathophysiology remains speculative for both syndromes: although both share factors of brain maturation, MAE is probably mainly related to genetic predisposition whereas LGS results from some unidentified cortical brain malformation. In unfavorable cases, there may therefore be a continuum between both syndromes. They need to be distinguished from other epilepsy syndromes and inborn errors of metabolism that begin in the same age range: atypical idiopathic benign epilepsy, frontal lobe epilepsy with secondary bisynchrony, ring chromosome 20, ceroid lipofuscinosis, and nonsymptomatic late-onset spasms.

Epileptic seizures are more frequent in the neonate than at any other time. The incidence of neonatal seizures (NNS) is estimated to be between 1.5 and 5.5/1000 living births, its onset being during the first week in 80% of cases. Mortality rate remains very high (20–45%). Not all paroxysmal manifestations are epileptic, and differential diagnosis remains an important challenge. Neonates may present with different types of seizures: clonic, tonic, myoclonic (axial, focal, erratic), epileptic spasms, and subtle seizures, including autonomic signs or automatisms. The main etiology is hypoxic–ischemic encephalopathy (40–45%) with a very early onset, and variable semiology including all seizure types. An EEG is necessary to recognize the seizures, and interictal tracing may help in assessing prognosis. Ischemic stroke is associated with seizures of early onset, being focal or unilateral. Interictal EEG is asymmetrical, with focal or unilateral patterns. Other etiologies less often linked to epileptic seizures must be looked for such as brain infection, metabolic disorders, chromosomal abnormalities, inborn errors of metabolism, brain malformations, and vitamin B6 dependency. Neonatal epilepsy syndromes may have favorable (benign familial neonatal seizures) or poor (early infantile encephalopathy with epilepsy, early myoclonic encephalopathy, and migrating partial seizures in infancy) prognosis.

In pediatrics recording of EEG can range from premature infants aged just 25 weeks of gestation to young adults. Recording EEG in pediatrics ranges from 25 weeks of gestation premature in the incubator to young adults. Hence, recording conditions need to be adapted to very different situations, not only of age but also of environment, asepsis, and behavior.This requires that recording conditions be adapted to very different situations, not only of age but also of environment, asepsis and behavior. The two major determinants of EEG features are the level of vigilance and age. Standard examination includes spontaneous sleep until the age of 5 years, and hyperventilation and intermittent light stimulation in older children. Hyperventilation may modify the tracing in a physiological way until adolescence. One of the major characteristics of a child's EEG recording is its course over time that parallels rapid brain maturation. EEG changes are particularly rapid in early age and they involve both temporal and spatial organization. In premature babies modifications appear by two 2 weeks, in infancy by 1 month and in childhood by 1 year, before reaching the adult patterns at an age varying between 8 and 12 years of age. Apart from being aware of the normal EEG patterns according to thein children of different ages, it is important to recognize unusual patterns that are not linked to a pathological situation. Most important are the interpretation and the conclusion of the EEG tracing and any conclusions reached, for which and a precise knowledge besides clinical information is mandatory for this purpose is essential.