Introduction

It is well recognized that children are at higher risk for seizures than adults (23, 24). In addition to the higher incidence of epilepsy in children than in adults, precipitating factors such as fever are far more likely to induce a seizure in a young child than in an adult. Children also have a significantly higher likelihood of entering remission than adults (8), further suggesting that the brain becomes less excitable with age. The results of animal studies parallel the results of clinical studies, with both indicating that the immature brain is more susceptible to seizures than the adult brain. Kindling, a process in which recurrent electrical stimulations initially produce only in brief electrical discharges and mild behavioral changes but, as the stimulations continue, result in more prolonged and intense electrical and behavioral seizures, occurs at all ages. Kindling occurs more rapidly in young animals than in mature animals (55). In addition, a shorter period of postictal refractoriness in young animals leads to a quick progression through the early stages of kindling and results in rapid generalization of seizures (26). Immature rats are also more likely to develop seizures with hypoxia than are mature rats (31).

Although the threshold for seizure generation is lower in immature than in adult brains, developing neurons are less vulnerable, in terms of neuronal damage and cell loss, than adult neurons to a wide variety of pathologic insults. For example, immature hippocampal neurons continue responding to synaptic stimuli in a fully anoxic environment for longer durations than adult ones (14). Similarly, longer anoxic episodes are required to irreversibly destroy the circuit in young animals (79). This reduced vulnerability is also reflected in the consequences of status epilepticus (SE). The pathophysiologic effects of SE are age-related, with both the morphologic and the behavioral consequences dependent on the age at SE onset.