TREATMENT OF CLUSTER SEIZURES STATUS EPILEPTICUS

摘要

The vast majority of seizures are self-limiting events, with eventual spontaneous return to resting or baseline neurologic function. However, during status epilepticus, a variety of changes occur within cells and networks of cells that result in a situation where the seizure activity becomes self-sustaining. These changes may be independent of the initiating cause of the seizure, and involves a variety of molecular mechanisms. Repetitive seizures cause inhibitory GABAA receptors to move from the synaptic membrane to the cell interior, while excitatory N-methyl-D-aspartate (NMDA) receptors may be recruited to the cell surface. Stores of inhibitory neurotransmitters may become depleted and increased expression of drug efflux transporters such as P-glycoprotein may occur. After a period of time, these cellular alterations may lead to pharmacoresistance to first-line agents that would normally be effective in seizure termination at earlier phases, such as the benzodiazepines.