Status epilepticus is common and associated with significant mortality and
complications. It affects approximately 50 patients per 100,000 population
annually and recurs in >13%. History of epilepsy is the strongest single ri
sk factor for generalized convulsive status epilepticus. More than 15% of p
atients with epilepsy have at least one episode of status epilepticus and l
ow antiepileptic drug levels are a potentially modifiable risk factor. Othe
r risks include young age, genetic predisposition, and acquired brain insul
ts. Fever is a very common risk in children, as is stroke in adults. Mortal
ity rates are 15% to 20% in adults and 3% to 15% in children. Acute complic
ations result from hyperthermia, pulmonary edema, cardiac arrhythmias, and
cardiovascular collapse. Long-term complications include epilepsy (20% to 4
0%), encephalopathy (6% to 15%), and focal neurologic deficits (9% to 11%).
Neuronal injury leading to temporal lobe epilepsy is probably mediated by
excess excitation via activation of The N-methyl-D-aspartate (NMDA) subtype
of glutamate receptors and consequent elevated intracellular calcium that
causes acute necrosis and delayed apoptotic cell death. Some forms of nonco
nvulsive status epilepticus may also lead to neuronal injury by this mechan
ism, but others may not. Based on clinical and experimental observations, c
omplex partial status epilepticus is more likely to result in neuronal inju
ry similar to generalized convulsive status epilepticus. Absence status epi
lepticus is much less likely to result in neuronal injury, and complication
s because it may be mediated primarily through excess inhibition. Future re
search strategies to prevent complications of status epilepticus include th
e study of new drugs (including NMDA antagonists,new drug delivery systems,
and drug combinations) to stop seizure activity and prevent acute and dela
yed neuronal injury that leads to the development of epilepsy.