Seizures result from excessive synchronized neuronal firing caused by imbalance between excitation (glutamate, AMPA/NMDA receptors) and inhibition (GABA). Epilepsy is a predisposition to recurrent seizures. Hyperexcitability stems from altered ion channels, reduced GABAergic tone, or excessive excitatory input.
Classify seizures by EEG pattern (generalized vs focal) and phenomenology (tonic-clonic, absence, focal motor). Understand status epilepticus as a medical emergency with risk of neuronal death.
Febrile seizures in childhood do not cause epilepsy in most cases—the risk is low. Photosensitivity is present in only ~3% of patients with epilepsy; it is not a universal trigger.
You already understand that neurons fire action potentials when sufficient excitatory input depolarizes them past threshold, and that GABAergic inhibition (via Cl⁻ influx through GABA-A receptors) counters glutamatergic excitation (via cation influx through AMPA and NMDA receptors). Normal brain function depends on keeping excitation and inhibition in dynamic balance. A seizure is what happens when that balance fails at scale — a population of neurons becomes abnormally synchronized and fires collectively in an uncontrolled burst, spreading electrical activity through connected circuits.
The threshold for this runaway excitation depends on several interacting mechanisms. Ion channel mutations are a major cause: altered voltage-gated sodium channels (as in SCN1A mutations causing Dravet syndrome) can either increase persistent sodium currents (more depolarization) or impair inhibitory interneuron function (less GABAergic brake). Reduced GABAergic tone can result from GABA receptor mutations, benzodiazepine withdrawal (which suddenly removes potentiation of GABA-A receptors), or alcohol withdrawal — all lower the threshold for synchronized firing. Metabolic derangements (hypoglycemia, hyponatremia, hypoxia) deprive neurons of the energy and ion gradients needed to maintain resting membrane potential, making the entire network more susceptible to runaway depolarization.
Not all seizures look or behave alike, because the location and spread of the abnormal discharge determines the clinical manifestation. Focal (partial) seizures begin in a discrete cortical region: a seizure starting in the primary motor cortex produces focal motor activity; one starting in the temporal lobe may produce déjà vu, complex automatisms, or altered awareness. If the discharge spreads to involve both hemispheres, the focal seizure secondarily generalizes, producing the characteristic tonic-clonic convulsion. Primary generalized seizures involve both hemispheres from onset — absence seizures show brief lapses of consciousness with 3-Hz spike-wave discharges on EEG; generalized tonic-clonic seizures involve a tonic phase (sustained muscular contraction, often with apnea) followed by a clonic phase (rhythmic jerking) followed by the postictal state (confusion, fatigue, often headache) as neurons recover from the metabolic exhaustion of the discharge.
Epilepsy is not a single disease but a predisposition to recurrent unprovoked seizures — it is diagnosed after at least two unprovoked seizures or one seizure with high recurrence risk. The word "unprovoked" matters: a seizure during meningitis, severe hypoglycemia, or alcohol withdrawal is a provoked seizure (the brain is reacting to an acute insult, not showing an intrinsic predisposition). Antiepileptic drugs work by stabilizing the excitation-inhibition balance through various mechanisms: sodium channel blockers (valproate, phenytoin) reduce repetitive firing; GABA potentiators (benzodiazepines, barbiturates) enhance inhibition; calcium channel modulators (ethosuximide) reduce thalamic burst firing in absence epilepsy. Status epilepticus — a prolonged seizure exceeding 5 minutes or recurrent seizures without recovery — is a medical emergency because sustained excitation exhausts neuronal energy metabolism, leading to excitotoxic cell death via calcium overload through NMDA receptors.