Clinical experience suggests two major components to the relationship between brain development and epilepsy. First, the maturational state of the immature brain appears to generally decrease seizure threshold and contribute to a different seizure phenotype from the adult. Second, certain forms of seizures, when present during development, may modify brain maturation to result in chronic epilepsy and/or other neurocognitive deficits.

Maturational studies in animals suggest there are numerous factors developmentally regulated in such a way as to increase excitability in immature neuronal networks in the forebrain. The developing brain appears to exhibit a transient overexpression of glutamate receptors, glutamate receptor subunit composition permissive of enhanced excitatory neurotransmission, a relative lack of GABAergic inhibitory transmission, and ion channel expression and homeostasis which enhance neuronal excitability. The increased excitatory “drive” that is likely to be critical for normal brain development may share common mechanisms with those responsible for rendering the immature brain more susceptible to seizures, seizure induced plasticity (epileptogenesis), and neuronal injury. Furthermore, the coincidence of seizures during early postnatal brain development may modify many of these parameters, which in turn may promote long term epilepsy.