1. Incidence, etiology and prognosis A large number of retrospective studies have shown that refractory persistent epilepsy accounts for approximately 31-43% of persistent epilepsy, but a prospective study from Lausanne/CH concluded that approximately 23% of patients with persistent epilepsy developed refractory persistent epilepsy after first-line and anticonvulsant medication use. This may vary considerably depending on the study population. Studies in children have shown that the duration of persistent status epilepticus is greater than 1 hour in 26-45%, greater than 2 hours in 17-25%, and greater than 4 hours in 10%. Population-based studies have found that children with persistent epilepsy have a higher proportion of emergency room visits with more than 60 minutes than the incidence of less than 60 minutes, and intensive care unit studies have reported a higher frequency of refractory persistent epilepsy than other studies, possibly related to the severity of suffering from refractory persistent epilepsy The prognosis of refractory persistent epilepsy is related to the etiology, clinical presentation, and age of the patient, and its short-term mortality The overall mortality rate is 16-39% and is as much as three times that of non-refractory status epilepticus, with severe neurological impairment in 39.1% and mild neurological impairment in 13% of cases. The majority of deaths in patients with refractory status epilepticus do not occur during the duration of status epilepticus, but rather afterwards, suggesting that the cause of death may be related to a number of underlying clinical factors. Etiology has been cited as one of the major independent factors affecting prognosis. The etiology can be divided into acute and chronic, with the former usually caused by discontinuation of antiepileptic drugs, which has a relatively good prognosis, and the latter, such as encephalitis, major stroke and rapidly progressive primary brain tumors, which are factors causing RSE with a poor prognosis. Systemic convulsive RSE can be associated with many complications, including cardiac arrhythmias, temperature dysregulation, electrolyte and glucose disturbances, rhabdomyolysis, and pulmonary edema. 2. Pathogenesis Most seizures terminate spontaneously within minutes, probably because of reactive γ -aminobutyric acid-mediated iatrogenic depression after a seizure. However, with persistent seizures, inhibitory γ-aminobutyric acid receptors are internalized into lattice-protein-coated vesicles, some of which are recycled to the cell membrane and some are disrupted in lysosomes, while excitatory NMDA receptors are mobilized to the cell membrane, and this receptor transport leads to reduced inhibitory control and increased excitability, which may result in persistent epileptic states. Alterations in neuropeptide and other gene expression after seizures lasting several hours may also contribute to the onset of persistent epilepsy. internalization of γ-aminobutyric acid receptors may explain the clinical finding that benzodiazepines, which act through a γ-aminobutyric acid mechanism, become less effective with increasing seizure duration and may suggest a role for the NMDA-regulating drug ketamine. The early treatment of refractory status epilepticus is based on the risk of RSE and the serious consequences of sustained seizures, and it is now widely recognized that RSE requires timely and effective pharmacological treatment. Studies have found that the treatment of SE is less effective as the duration of seizures lengthens. One antiepileptic drug is 55% effective for convulsive seizure continuity, while a second or third drug is less than 10% effective. A study of rats with persistent epilepsy induced by repeated electrical stimulation of limbic structures found that benzodiazepines and phenytoin sodium were effective in the early stages of seizures, and over time SE became resistant to these drugs but became highly effective against antagonists of NMDA receptors; other animal experiments also found internalization of GABAa receptors into the cytoplasm, and these findings provide a basis for successful pharmacological control of refractory persistent epilepsy These findings provide a basis for the choice of treatment for the successful control of refractory persistent epilepsy.