Seizures happen when nerve cells in the brain fire in a sudden, uncontrolled burst of electrical activity. The causes range from temporary disruptions like low blood sugar or a high fever to chronic conditions like epilepsy or brain injury. Understanding the trigger matters because some causes are one-time events that resolve on their own, while others signal an ongoing risk that needs management.
How the Brain Loses Control
Your brain runs on a tightly regulated balance between signals that excite nerve cells and signals that calm them down. The main excitatory chemical messenger is glutamate, which tells neurons to fire. The main inhibitory one is GABA, which tells them to stop. When this balance tips too far toward excitation, neurons can begin firing together in rapid, synchronized bursts. That’s a seizure.
This imbalance can happen in several ways. Sometimes the brain produces too much glutamate or fails to clear it quickly enough from the spaces between neurons. In animal studies, when the cleanup system for glutamate was genetically removed from brain cells, the excess glutamate triggered spontaneous seizures severe enough to be fatal within weeks. Other times, GABA signaling is too weak to keep excitatory activity in check. Many seizure medications work by boosting GABA’s calming effect or reducing glutamate’s excitatory push.
Metabolic and Chemical Triggers
Some seizures are “provoked,” meaning a temporary chemical disruption in the body pushed the brain past its threshold. These are not epilepsy. They’re the brain’s response to an acute problem, and they typically don’t recur once that problem is corrected.
Low blood sodium (hyponatremia) is one of the most common metabolic triggers. Seizures generally occur when sodium drops rapidly below 115 milliequivalents per liter, though symptoms can appear at levels around 110 to 120. Low blood sugar is another classic trigger, particularly in people with diabetes who take insulin. Other electrolyte imbalances that can provoke seizures include severely low calcium, severely low magnesium (typically below 1 milliequivalent per liter), and very high sodium levels above 158 to 160. In each case, the electrolyte disturbance disrupts the electrical environment neurons need to function normally.
Alcohol and Drug Withdrawal
Alcohol withdrawal is one of the more common causes of provoked seizures in adults. When someone who has been drinking heavily for a prolonged period suddenly stops, the brain rebounds into a state of hyperexcitability. Chronic alcohol use suppresses brain activity over time, and the brain compensates by increasing its baseline excitatory tone. Remove the alcohol, and that heightened excitability has nothing to counterbalance it.
Withdrawal seizures most commonly appear 6 to 48 hours after the last drink, and more than 90% occur within the first 48 hours. These are typically generalized tonic-clonic seizures, meaning they involve stiffening and rhythmic jerking of the whole body. Withdrawal from benzodiazepines and barbiturates can produce seizures through a similar rebound mechanism.
On the other side of the equation, certain drugs can directly lower the seizure threshold. Cocaine, amphetamines, and synthetic stimulants are well-known triggers. So are certain prescription medications at toxic doses.
Febrile Seizures in Children
Febrile seizures are the most common type of seizure in young children, typically occurring between 6 months and 5 years of age. They happen alongside a fever above 100.4°F (38°C), but there’s no single temperature that triggers them. Each child has a different convulsive threshold, and for some, a relatively modest fever is enough.
Simple febrile seizures are a single episode lasting less than 15 minutes. Complex febrile seizures last longer than 15 minutes, occur more than once within 24 hours, or involve only one side of the body. Simple febrile seizures, while frightening for parents, do not cause brain damage and do not mean a child has epilepsy. Most children outgrow them entirely.
Structural Brain Damage
Anything that physically damages brain tissue can create a focus of abnormal electrical activity. This includes stroke, brain tumors, brain infections, and traumatic brain injury (TBI). The more severe the damage, the higher the seizure risk.
After severe TBI, about 25% of patients develop epilepsy within five years, and that number climbs to 32% by fifteen years. Once a first post-traumatic seizure occurs, the risk of additional seizures is high: 61% at two years and 82% at ten years. Injuries involving bleeding into the brain, damage to the cortex (the brain’s outer layer), or large areas of tissue loss carry the greatest risk.
Stroke is the leading recognized cause of new-onset seizures in adults over 65. Strokes that involve the cortex, that are hemorrhagic (bleeding rather than clot-based), or that affect large areas of the brain are especially likely to provoke seizures. Dementia also raises risk: seizures have been reported in about 7% of people with clinically probable Alzheimer’s disease.
Infections That Affect the Brain
Infections that reach the brain or its surrounding membranes can trigger seizures acutely or leave lasting damage that leads to epilepsy. Meningitis, encephalitis, and brain abscesses are all potential causes. In many low- and middle-income countries, a parasitic infection called neurocysticercosis, caused by pork tapeworm larvae lodging in the brain, accounts for roughly 30% of all acquired epilepsy cases in regions where the parasite is common.
Genetic Factors
Some people are born with a genetic predisposition to seizures. Mutations in genes that code for sodium or potassium channels in neurons, or for GABA receptors, can make the brain inherently more excitable. These genetic epilepsies often appear in childhood.
Dravet syndrome is one of the most well-characterized genetic epilepsies. About 80% of cases are caused by mutations in a gene called SCN1A, which provides instructions for building sodium channels in nerve cells. When these channels don’t work properly, neurons fire too easily. Mutations in over a dozen other genes, including those affecting GABA receptors and other ion channels, can produce similar seizure disorders.
Sleep Deprivation
Missing sleep is a well-established seizure trigger, particularly in people who already have epilepsy. Sleep deprivation reduces the brain’s inhibitory signaling. Studies using brain stimulation techniques have shown that sleep loss decreases intracortical inhibition and increases excitability in people with both focal and generalized epilepsy. At the cellular level, sleep deprivation weakens the brain’s tonic inhibition, the steady background calming current that GABA receptors normally provide, making neurons more likely to fire out of control.
This is why neurologists emphasize consistent sleep schedules for people with seizure disorders. Even a single night of significantly shortened sleep can be enough to provoke a seizure in someone whose threshold is already low.
Flashing Lights and Visual Patterns
About 3% of people with epilepsy have photosensitive epilepsy, where specific visual stimuli can trigger a seizure. Flashing lights between 5 and 30 flashes per second (hertz) are the most likely to provoke one, with safety guidelines recommending that sensitive individuals avoid flashes faster than 3 per second. Moving or static striped patterns can have the same effect because the alternation of light and dark areas mimics a flashing stimulus to the brain. High-contrast images, where bright and dark areas differ sharply, increase the danger.
This is why video games, concerts, and certain television broadcasts carry photosensitivity warnings. The famous 1997 episode of the Pokémon animated series that hospitalized hundreds of children in Japan involved rapidly flashing red and blue images at a frequency squarely in the danger zone.
Why Seizure Threshold Varies
Everyone has a seizure threshold, the point at which abnormal electrical activity overwhelms the brain’s ability to contain it. Some people have a naturally low threshold due to genetics, brain injury, or a neurological condition, meaning it takes less provocation to trigger a seizure. Others have a high threshold and may never experience one despite exposure to common triggers.
Most seizures result from a combination of factors rather than a single cause. Someone with a mildly lowered threshold from a family history of epilepsy might go their whole life without a seizure, unless they combine sleep deprivation with heavy alcohol use on a night with flashing strobe lights. The triggers stack. This is why identifying and managing individual risk factors, even seemingly minor ones like inconsistent sleep, can make a meaningful difference in seizure control.