Overview
Clinical Meaning
Seizures result from abnormal, excessive, synchronous neuronal discharge in the cerebral cortex.
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.