A seizure happens when neurons in the brain fire electrical signals in an uncontrolled, synchronized burst. Normally, brain cells communicate through carefully balanced waves of electrical and chemical activity. During a seizure, that balance breaks down, and large groups of neurons start firing together at once, overwhelming the brain’s normal function. About 8% to 10% of people will experience at least one seizure in their lifetime.
The Chemical Balance That Keeps Neurons in Check
Your brain runs on two opposing chemical systems. One uses a signaling molecule called glutamate, which excites neurons and tells them to fire. The other uses a molecule called GABA, which quiets neurons down and tells them to stop. Think of it as a gas pedal and a brake. In a healthy brain, these two forces stay roughly in balance, so electrical signals travel in orderly patterns.
A seizure begins when that balance tips toward too much excitation. This can happen because glutamate signaling ramps up, GABA signaling weakens, or both occur at the same time. When glutamate locks onto a receiving neuron, it opens tiny channels in the cell membrane that let charged particles (sodium and calcium) rush in, making the neuron more electrically charged and more likely to fire. GABA normally counteracts this by opening channels that let different charged particles (chloride) flow in, dampening the signal. If GABA’s braking system fails, or if glutamate floods the gaps between neurons, the excitation spreads unchecked.
In some forms of epilepsy, the GABA system doesn’t just weaken. It actually reverses. Changes in the way cells handle chloride can flip GABA’s effect so that it excites neurons instead of calming them. That’s like pressing the brake and having the car accelerate.
How Ion Channels Malfunction
The electrical behavior of every neuron depends on tiny protein gates called ion channels, which open and close to let charged particles move in and out of the cell. Different types of channels handle sodium, potassium, and calcium. When any of these channels malfunction, whether from a genetic mutation, an injury, or a disease process, neurons can become hyperexcitable.
Sodium channels are especially important. In some epilepsy syndromes, sodium channels in the brain’s inhibitory neurons (the ones that normally slow things down) stop working properly. This silences the brain’s own braking system, leaving excitatory neurons free to fire without restraint. In other cases, sodium channels in excitatory neurons get stuck partially open, creating a persistent inward current that keeps the neuron in a hair-trigger state.
Potassium channels play the opposite role. They help neurons reset after firing by letting positive charge flow back out of the cell. When potassium channels are reduced or damaged, neurons recover more slowly and fire more readily. Calcium channel problems contribute too. Certain mutations increase a type of low-voltage calcium current that makes neurons fire in rapid bursts, a pattern characteristic of some absence seizures that involve a back-and-forth loop between the brain’s deep relay centers and the cortex.
Focal vs. Generalized Seizures
Where the abnormal firing starts, and how far it spreads, determines the type of seizure. A focal seizure begins in one specific area of the brain. If it starts in the region controlling your right hand, for instance, you might notice involuntary twitching in that hand while remaining fully aware. Focal seizures can stay confined to one area or spread across the brain, eventually becoming a full-body convulsive event.
A generalized seizure involves both hemispheres of the brain from the very beginning. Absence seizures, where a person stares blankly for a few seconds, are generalized. So are tonic-clonic seizures (formerly called grand mal), where the body stiffens and then jerks rhythmically. The distinction between focal and generalized isn’t always clean. EEG recordings sometimes show seizures that start with widespread activity and then settle into one region, or focal seizures that spread so quickly they look generalized from the start. In one study, nearly half of patients with a focal onset showed the abnormal activity spreading to both hemispheres.
What the Brain Looks Like on EEG
An electroencephalogram (EEG) records the brain’s electrical activity through sensors placed on the scalp, and seizures produce distinctive patterns. Between seizures, the brain of someone with epilepsy often shows sharp spikes or “spike-and-wave” complexes: a brief electrical spike lasting 20 to 70 milliseconds followed by a slower wave. These are generated by clusters of neurons within the seizure-prone area firing in sync.
Different seizure types produce recognizable signatures. Childhood absence epilepsy shows a characteristic 3-per-second spike-and-wave rhythm. Myoclonic epilepsy produces bursts of multiple rapid spikes followed by slow waves. A common childhood epilepsy called benign Rolandic epilepsy shows spikes concentrated over the area of the brain that controls the face and tongue. During an active seizure, these patterns become continuous and rhythmic, replacing the brain’s normal background activity.
Common Triggers That Lower the Threshold
Everyone has a seizure threshold, a point at which the brain’s normal safeguards are overwhelmed. In people with epilepsy, that threshold is already lower than average, and certain factors can push it lower still. Even people without epilepsy can seize if the provocation is strong enough.
The most commonly reported triggers include:
- Sleep deprivation, which is one of the most reliable seizure triggers
- Stress, whether emotional or physical
- Alcohol, particularly heavy use or withdrawal
- Flashing lights or visual patterns, which affect a subset of people with photosensitive epilepsy
- Illness or fever
- Missed meals, dehydration, or low blood sugar
- Hormonal changes, especially around menstruation
- Missed medications in people already taking anti-seizure drugs
- Recreational drugs, particularly stimulants like cocaine
When Body Chemistry Itself Causes a Seizure
Some seizures aren’t caused by an underlying brain disorder at all. They’re provoked by a temporary metabolic crisis. These are called acute symptomatic seizures, and they can happen to anyone.
Sodium imbalances are a major culprit. When blood sodium drops significantly below normal (a condition called hyponatremia), the brain swells, and as the imbalance worsens, confusion gives way to seizures. High blood sodium is dangerous too, and correcting it too quickly can itself trigger seizures by causing rapid fluid shifts in the brain.
Blood sugar extremes work similarly. Up to 25% of people with severely high blood sugar may experience seizures, often focal motor seizures that cause jerking on one side of the body. Severely low blood sugar triggers seizures in roughly 7% of cases. Calcium imbalances in either direction, whether too high or too low, can also provoke seizures by directly altering how excitable neurons are.
The Three Phases of a Seizure
A seizure isn’t just the visible event. It unfolds in stages, and understanding them helps you recognize what’s happening.
Before: The Prodrome and Aura
Some people notice warning signs hours or even days before a seizure. This prodrome phase can include mood changes, anxiety, lightheadedness, trouble concentrating, or disrupted sleep. Not everyone experiences it, but those who do often learn to recognize it as a reliable signal. An aura, which is technically a small focal seizure itself, may occur in the seconds before a larger seizure. It can involve unusual smells, a rising feeling in the stomach, déjà vu, or visual disturbances.
During: The Ictal Phase
The ictal phase is the seizure itself. It typically lasts from a few seconds (in absence seizures) to one or two minutes (in tonic-clonic seizures). During this phase, the synchronized electrical storm dominates the affected brain regions, producing the outward symptoms: staring, muscle stiffening, rhythmic jerking, loss of awareness, or a combination of these. A seizure lasting five minutes or more without stopping is classified as a medical emergency called status epilepticus, which requires immediate treatment to prevent brain injury.
After: The Postictal State
Once the seizure ends, the brain doesn’t snap back to normal. The postictal state is a recovery period driven by neuronal exhaustion and a rebound surge of inhibitory activity. The brain essentially slams on the brakes to stop the seizure, using mechanisms like depleting its supply of glutamate, releasing natural calming compounds (including the brain’s own versions of cannabinoids and opioids), and ramping up GABA signaling.
Blood flow to the area where the seizure originated roughly doubles within five minutes of the event, then drops below baseline after about an hour. This helps explain the progression of postictal symptoms: initial confusion and disorientation, followed by fatigue, headache, muscle soreness, and sometimes difficulty speaking or thinking clearly. The postictal state can last anywhere from minutes to hours, and occasionally a day or more after a severe seizure. Some people fall into a deep sleep. Others feel emotionally fragile or struggle to form new memories for a period afterward.