Status epilepticus

Status epilepticus is a seizure lasting long enough to require urgent treatment, or repeated seizures without recovery between them. It can cause lasting brain injury or death.

Seizure: A transient episode of abnormal, excessive or synchronous neuronal activity in the brain. Status epilepticus is defined by seizure activity that persists or recurs without recovery.
Benzodiazepine: A class of drugs that enhances signaling at GABA-A receptors and can suppress seizures. Benzodiazepines are first-line emergency medicines for many convulsive episodes.
Convulsive status epilepticus: Status epilepticus involving sustained or recurrent convulsions without recovery between seizures. This visible form is a time-critical emergency and often defines public understanding of the condition.
Epilepsy: A chronic brain disorder characterized by an enduring predisposition to epileptic seizures. Status epilepticus is an emergency event, not a synonym for the chronic disorder.
Excitotoxicity: Neuronal injury caused by excessive activation of excitatory receptors, often through glutamate. Prolonged seizure activity can overstimulate neurons and contribute to brain injury.
Midazolam: A short-acting benzodiazepine used for sedation and emergency seizure treatment. It is commonly used when rapid treatment is needed outside a hospital.
Nonconvulsive status epilepticus: Ongoing seizure activity without prominent convulsions, often presenting as altered awareness or behavior. It can persist unnoticed unless EEG is used to identify seizure activity.
Psychogenic non-epileptic seizure: An episode resembling an epileptic seizure that is not caused by epileptic electrical activity. It can resemble convulsive status, but its cause and treatment differ.
GABA receptor: A receptor that responds to gamma-aminobutyric acid, the brain's principal inhibitory neurotransmitter. Reduced inhibitory signaling helps explain why prolonged seizures can become harder to stop.
Levetiracetam: An antiseizure medicine that binds synaptic vesicle protein SV2A and alters neurotransmitter release. It is one option for ongoing treatment after initial benzodiazepines fail.

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