Pathophysiology

The exact mechanism of febrile seizures is unknown but fever lowers the seizure threshold in the developing brain. Febrile seizures likely result from the immature brain’s inability to compensate for the physiological changes of fever. There is no clear evidence that febrile seizures cause permanent neuronal damage or structural abnormalities in the brain. The slightly increased risk of future epilepsy is likely from genetic predisposition rather than brain injury from the seizures themselves.

Status epilepticus results from failure of the body’s endogenous mechanisms to terminate seizure activity. An imbalance occurs between excitatory neurotransmitters like glutamate and inhibitory ones like GABA. With prolonged seizure activity, GABA receptors undergo structural changes causing benzodiazepine resistance. Unopposed glutamate excitation leads to neuronal injury and death via mitochondrial dysfunction. Metabolic changes include increased glucose utilization, lactic acidosis, hyperthermia, and autonomic instability.