Seizures result from abnormal, excessive, synchronous neuronal discharge in the cerebral cortex. The balance between excitatory (glutamate, NMDA/AMPA receptors) and inhibitory (GABA, chloride channel) neurotransmission is disrupted. In focal seizures, a discrete cortical focus generates paroxysmal depolarization shifts (PDS) — sustained depolarization driven by calcium influx through NMDA receptors, followed by GABA-mediated hyperpolarization. When inhibitory surround fails, the seizure propagates. Generalized seizures involve bilateral hemispheric networks from onset, often through thalamocortical circuits. Status epilepticus (SE) occurs when seizure-terminating mechanisms fail: GABA-A receptor internalization begins within 5 minutes of continuous seizure activity, while NMDA receptor expression increases on the cell surface — this explains why benzodiazepines become less effective and why treatment urgency is paramount. After 30 minutes of SE, excitotoxic neuronal death begins, with hippocampal neurons being most vulnerable.