SE occurs when the brain fails to stop an isolated seizure. The exact reason for this failure is unknown and probably involves multiple mechanisms. A seizure is likely to occur due to a mismatch of excitatory and inhibitory neurotransmitters in the brain. The primary excitatory neurotransmitter is glutamate. Glutamate stimulates postsynaptic #-methyl-D-aspartate (NMDA) receptors, causing an influx of calcium into the cells and depolarization of the neuron. Sustained depolarization may maintain SE and eventually cause neuronal injury and death.6 The primary inhibitory neurotransmitter, Y-aminobutyric acid (GABA), opposes the excitatory response by stimulating GABAa receptors, enhancing chloride inhibitory currents, producing hyperpol-

arization, and inhibition of the postsynaptic cell membrane. The inhibitory ability of GABA diminishes as the duration of seizures increases, perhaps due to a mechanistic shift in the functional properties of the GABAa receptors, which causes a decrease

in response to GABA-receptor agonists. ' Seizures lasting more than 30 minutes can cause injury and neuronal loss in the hippocampal, cortical, and thalamic regions. These neurologic sequelae are related to the excessive electrical activity and alterations in cerebral metabolic demand. The clinical impact of the GABAA-receptor changes on treatment response and the worsening degree of neuronal injury with prolongation of seizure activity highlights the urgency of rapid control of SE.

Several systemic changes occur in two phases during the course of SE. Phase I occurs during the first 30 minutes of seizure activity, and phase II occurs after 30 minutes of seizure activity.9

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