What Happens in a Seizure
A seizure is an electrical storm. Normally your brain balances excitation (glutamate) against inhibition (GABA), so neurons fire in tidy, independent patterns. Watch that balance here as a living network of neurons. Then tip it: let one patch become hyperexcitable, and instead of the surrounding brake damping it, the firing turns synchronous — the neurons stop doing their own jobs and all fire together. If it stays put it is a focal seizure; if it recruits the whole brain it becomes a generalised one. The EEG below is the same storm, read from the scalp.
Try this: start on Normal and watch the Synchrony readout hover near zero — every neuron on its own clock. Now press ⚡ Provoke a seizure and watch a single focus lock the whole network into one rhythm, the EEG blow up into rhythmic spikes, then hit Medication to restore the brake and calm the storm.
Live seizure readout
What’s happening
The animation is an illustrative model, not a recording of one person’s brain. The mechanism is real — excitation/inhibition balance, hyperexcitability, hypersynchrony, focal vs generalised spread, and the EEG spike-and-wave signature. The exact neuron count, firing rates and the “synchrony” number are a simplified simulation to make the idea visible, not clinical measurements.
The Science in Plain Language
1. Your brain runs on a balance
At every instant, billions of neurons are shouting go and stop at each other. The main “go” signal is the neurotransmitter glutamate, which excites the next cell through AMPA and NMDA receptors. The main “stop” signal is GABA (gamma-aminobutyric acid), which opens chloride channels on the GABA-A receptor and quiets the next cell. Roughly one in five cortical neurons is an inhibitory interneuron whose entire job is to hold the excitatory majority in check. When those two forces are matched, the network stays lively but desynchronised — each neuron doing its own job. That balance is the whole story of this page.
2. A seizure is hyperexcitability plus hypersynchrony
Two things have to go wrong at once. First, a group of neurons becomes hyperexcitable — too easy to fire, because the brake is too weak or the accelerator too strong. Second, and this is the part people miss, they start firing in synchrony: instead of a healthy babble of independent voices, thousands of cells discharge at the same instant, over and over. Notice in the animation that individual firing rates barely change — the Synchrony readout is what explodes. That hypersynchronous discharge is a seizure. Neurologists literally measure it as neurons “phase-locking” together, which is exactly what the synchrony number here is modelling.
3. Focal vs generalised — where it is decides what you feel
A focal seizure stays in one patch of cortex, so the symptom matches that patch’s day job. A focus in the motor strip gives a twitching hand; in the temporal lobe it can give a rising stomach feeling, a strange smell, a wave of déjà vu or intense fear. The person may stay fully aware (a “focal aware” seizure, once called simple partial) or lose awareness. A generalised seizure engulfs both hemispheres at once, so consciousness goes immediately. Press Spread and watch the recruitment ring turn a local event into a whole-brain one — that transition, called secondary generalisation, is the moment a focal seizure becomes a convulsion.
4. The tonic-clonic seizure, explained
The dramatic whole-body convulsion is a generalised tonic-clonic seizure (the old term was grand mal). In the tonic phase every motor pathway fires at once, so the muscles stiffen — the person may cry out as air is forced past the vocal cords, and they fall. In the clonic phase the massed inhibitory neurons periodically interrupt the storm, chopping the sustained contraction into the rhythmic jerking. When the inhibitory networks finally exhaust the discharge, the brain crashes into a post-ictal state — deep confusion, sleepiness, sometimes sore muscles or a bitten tongue — that can last minutes to hours. Not every seizure looks like this: absence seizures are just a few seconds of blank staring with a 3-per-second spike-wave EEG, and many focal seizures never involve a single jerk.
5. What tips the balance — the causes
Epilepsy is the tendency to have recurrent, unprovoked seizures, and it affects roughly 50 million people worldwide; about 1 in 26 people will develop it at some point in life. The causes fall into a few families. Genetic / ion-channel: mutations in the very channels that shape the nerve impulse — the sodium-channel gene SCN1A (mutated in Dravet syndrome), potassium-channel genes like KCNQ2, and GABA-receptor genes like GABRG2 — make neurons intrinsically over-excitable. Structural: a scar from a stroke, a brain tumour, a head injury, a developmental malformation, or scarring of the hippocampus (mesial temporal sclerosis) creates a local zone that fires abnormally. Metabolic and autoimmune causes and CNS infections round out the list. In many people no single cause is ever found.
6. Triggers — the same balance, pushed
A trigger doesn’t cause epilepsy; it lowers the threshold on a brain that is already prone. The big ones are remarkably ordinary: missed sleep, skipped medication, alcohol — especially withdrawal the morning after, low blood sugar, physical or emotional stress, and in a minority of people, flashing lights or striking patterns (photosensitive epilepsy, only about 3% of people with epilepsy — far rarer than films suggest). In young children a fever can trigger a febrile seizure; these affect a few per cent of children between about 6 months and 5 years, are usually brief and benign, and most children outgrow them without developing epilepsy. Each trigger nudges the excitation/inhibition balance the animation is built around.
7. How anti-seizure medicines restore the brake
Every anti-seizure drug is, in effect, re-balancing this page. Some boost inhibition: benzodiazepines (lorazepam, diazepam — the rescue drugs) and phenobarbital enhance the GABA-A receptor; vigabatrin and tiagabine raise GABA levels. Others damp excitation by blocking the sodium channels that carry the runaway firing — carbamazepine, lamotrigine, phenytoin, lacosamide — or by blocking calcium channels: ethosuximide targets the T-type calcium current behind absence seizures. Levetiracetam (Keppra) works on the synaptic-vesicle protein SV2A, and broad-spectrum valproate hits several of these at once. Press Medication in the diagram: inhibition climbs, coupling falls, and the synchronised storm dissolves back into independent firing. For roughly two-thirds of people, the right drug controls seizures well.
8. The myth worth correcting
The most dangerous myth is that you should put something in the mouth of someone having a seizure, or hold them down. Do neither. It is physically impossible to “swallow your tongue,” and forcing objects or fingers into the mouth breaks teeth, causes bites, and can block the airway. The real first aid is simple: protect the head, move hard objects away, turn the person on their side, time it, and stay until they recover. A second myth: epilepsy is not a mental illness and is not a mark of low intelligence — most people with epilepsy have entirely typical cognition and lives. And a seizure is not always a convulsion; a blank stare or a strange rising smell can be one too.
9. When it becomes an emergency
Most seizures stop on their own within 1 to 3 minutes. A seizure lasting 5 minutes or longer, or seizures that repeat without the person recovering in between, is called status epilepticus — a medical emergency. The longer the brain fires, the harder it is to stop and the greater the risk of injury, so the rule of thumb is to call emergency services if a convulsive seizure passes the 5-minute mark, if breathing doesn’t recover, if it’s a first-ever seizure, or if it happens in water, in pregnancy, or after a serious injury. Rescue medicines — usually a benzodiazepine given into the cheek, nose or rectum — are designed to break the storm before it becomes self-sustaining, which is exactly the transition you can watch tip over in the Spread scenario.