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The possible deleterious role of febrile seizures on development is an old issue. It took a long time to realize that impaired development or occurrence of chronic epilepsy affected a very small minority of children with febrile seizures. These children either had pre-existing brain damage, specific genetic epileptic conditions, or seizure-induced brain damage from repeated prolonged seizures. Population-based (and not hospital-based) large prospective studies of children with simple febrile seizures (a definition that is still debated) have quite unequivocally shown that these do not cause any brain injury.

Children with ‘simple’ febrile seizures do not differ from controls in intelligence and behaviour at school age1,2 and the large majority do not develop epilepsy.3 So why another study on this topic and are there new data challenging what most clinicians thought was a settled issue?

Visser et al.’s 4article comes from a large population-based cohort in which seizure data were assessed by questionnaires at the ages of 1, 2, and 3 years. They distinguished children with single versus recurrent febrile seizures, the latter defined as more than one single febrile seizure (number, focality, and duration of seizures were not studied). They found in both groups that social-behavioral development at 3 years (Child Behavior Checklist [CBCL]) and a comprehensive questionnaire on executive functions (Behavior Rating Inventory of Executive Function-Preschool Version [BRIEF-P]) at 4 years were not different from that of controls without seizures. These findings also applied to the 23 children whose first febrile seizure had occurred before the age of 1 year, contrary to some previous studies. All this is confirmatory good news.

However, there was one new finding in children with recurrent seizures. The authors found ‘an increased risk of delayed vocabulary development’ on the basis of the language questionnaire at 2.5 years (not checked at 4y). They concluded that ‘children with recurrent febrile seizures might be at risk for delayed language development.’ The authors proposed that some brain dysfunction related to the febrile seizure could occur, because their onset coincides with rapid language acquisition between 1 year and 3 years. Knowing the variability of language development, and especially expressive speech (here vocabulary at the age of 2.5y), the relevance of this statistical difference is questionable. It is more likely that children with recurrent febrile seizures and language delay are a heterogenous population with, among others, specific genetic conditions, or pre-existing brain pathology.

The results of this study do not challenge older data showing that febrile seizures do not have developmental consequences.

Nowadays, clinicians who see a child with a first seizure while febrile will integrate new data that have changed the old dichotomous vision of simple versus complex febrile seizures. This event is now regarded as having a much broader range of possible causes, mainly brain susceptibility due to different genes (e.g. SCN1A, SCN2A, PCDH19), a viral infection with propensity to seizures with fever (e.g. Rota-virus infection), or a symptomatic epilepsy with normal development. The clinical context will sometimes suggest specific epileptic syndromes such as infantile familial convulsions, Dravet syndrome, idiopathic partial epilepsies, or generalized or genetic epilepsy with febrile seizures plus (GEFS+). The latter (GEFS+) seems more frequent than initially thought and has most often a benign prognosis. An occasional afebrile seizure or a family history of epilepsy in close relatives in a child with otherwise simple febrile seizures is now looked at with this possibility in mind.

The rare cases with one or several severe recurrences (status) are now less frequent and better handled by the parents at home with rectal or oral short-acting diazepines (midazolam) with a decreased risk of seizure-induced brain damage. Much progress has been made since the time when prophylactic phenobarbital was proposed for children at the first or second febrile seizure. The spectrum of conditions under what seemed a simple genetic transitory childhood condition or epilepsy triggered by fever has been much enlarged.

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