Pathophysiology
Clinical meaning
Seizures result from abnormal, excessive, and synchronous neuronal electrical discharge in the cerebral cortex. The balance between excitatory (glutamate/NMDA) and inhibitory (GABA) neurotransmission maintains normal cortical function. Seizures occur when this balance shifts toward excitation through increased glutamatergic transmission, decreased GABAergic inhibition, or altered intrinsic neuronal membrane properties (channelopathies affecting sodium, potassium, or calcium channels). Focal seizures originate in a localized cortical region: focal aware (consciousness preserved, formerly simple partial), focal impaired awareness (consciousness altered, formerly complex partial), and focal to bilateral tonic-clonic. Generalized seizures involve both hemispheres from onset: absence (3 Hz spike-and-wave on EEG), myoclonic, tonic, atonic, and tonic-clonic. Status epilepticus is defined as continuous seizure activity lasting >= 5 minutes or two or more seizures without full recovery of consciousness, constituting a neurological emergency with increasing neuronal death, excitotoxicity, and systemic complications (rhabdomyolysis, hyperthermia, respiratory failure).