Seizures result from abnormal, excessive, and synchronous neuronal discharge in the cerebral cortex caused by an imbalance between excitatory (glutamate) and inhibitory (GABA) neurotransmission. The balance tips toward excitation through several mechanisms: increased glutamate release, enhanced NMDA/AMPA receptor sensitivity, decreased GABAergic inhibition, or altered ion channel function (channelopathies). Focal seizures originate from a localized cortical region and produce symptoms reflecting that area's function (e.g., temporal lobe = automatisms, déjà vu, olfactory hallucinations; frontal lobe = motor activity). Generalized seizures involve both hemispheres from onset through thalamocortical circuits. Tonic-clonic seizures involve initial tonic phase (sustained muscle contraction from synchronous cortical discharge, 10-20 seconds) followed by clonic phase (rhythmic contracting and relaxing from alternating excitatory and inhibitory volleys, 30-60 seconds). Status epilepticus (seizure lasting >5 minutes or recurrent seizures without recovery) represents a neurological emergency where excitatory mechanisms overwhelm inhibitory controls, GABA receptors are internalized from the membrane, and progressive neuronal injury occurs from metabolic exhaustion, hyperthermia, and excitotoxicity.