Issues in paediatric epilepsy

Epilepsy is the most common chronic neurological disorder of childhood, encountered by both general paediatricians and paediatric neurologists. The incidence of epilepsy is approximately seven to eight new cases per 1000 per year in children under the age of 11 years (1). Correct diagnosis and appropriate classification are crucial for the overall management of children with epilepsy, including both the type of seizure and the epileptic syndrome, based on clinical findings and the pattern of the interictal and, whenever possible, the ictal electroencephalogram (EEG). Despite recent advances in pharmacological therapy and the development of an improved classification system, over 25% of children diagnosed with epilepsy still remain refractory to drug therapy (2). Paediatric epilepsy has specific characteristics in early life. Seizures in neonates do not seem to severely damage the brain per se, although they are often a manifestation of brain damage, such as arterial ischaemic stroke (3, 4). Later in life, particularly in infancy, seizures may produce damage if they are prolonged, febrile and focal, increasing the risk for intractable epilepsy and other neurological sequelae. Although 10–20% of children with acute symptomatic neonatal seizures develop epilepsy later in life, antiepileptic drug (AED) treatment should be discontinued on leaving the neonatal unit, unless seizures and/or spikes persist. In addition, family counselling and anticipatory medical care after discharge are also important issues to take into account, particularly the description of various types of seizures that may be difficult to recognize clinically. In paediatric patients, epileptic encephalopathies characterized by early continuous interictal spike and slow wave activity combined with cognitive and/or motor dysfunction require vigorous treatment of the epilepsy in order to establish adequate seizure control as soon as possible (5). Age-related characteristics of epilepsy syndromes result from differential maturation of the neocortex, from perisylvian to occipital and then frontal. Moreover, in many instances, subcortical structures as well as the cortex may also be involved. Although mesial temporal areas mature early, their functional connection to other neocortical areas is delayed by several years; this could explain how early damage may produce late epilepsy.