Abstract
Recurrent or prolonged seizures cause selective neuronal injury in vulnerable structures in animal models and in humans. Considerable evidence suggests that seizure-induced neuronal injury is epileptogenic. For example, a large fraction of animals that experience chemoconvulsant-induced status epilepticus and associated neuronal loss in limbic structures go on to develop spontaneous recurrent seizures. In contrast to adult animals, immature animals manifest little, if any, neuronal injury after status epilepticus. We and others have shown that even in the absence of seizure-induced injury, animals that experience status epilepticus, when immature, manifest enhanced injury and an enhanced behavioral response to status epilepticus later in life. We have termed this the two-hit phenomenon: a single apparently noninjurious event confers enhanced vulnerability to later life events. The mechanism of the two-hit phenomenon remains uncertain.
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