What is epilepsy?

A seizure is not the same as epilepsy

The brain works thanks to millions of neurons that communicate through tiny electrical signals. An epileptic seizure happens when a group of neurons becomes active in an excessive, synchronized way — all at once — for a short time. Depending on which part of the brain is involved, a seizure can cause movements, strange sensations, a brief loss of contact with the surroundings, or loss of consciousness.

Having a seizure does not necessarily mean having epilepsy. Many seizures are provoked by a specific cause — for example, a high fever in young children, very low blood sugar, or suddenly stopping alcohol — and do not happen again once that cause is gone.

Epilepsy is a disease of the brain characterized by a lasting tendency to generate seizures. In practice, the International League Against Epilepsy (ILAE) considers that a person has epilepsy if any of the following applies:1

• they have had at least two unprovoked seizures more than 24 hours apart;
• they have had one unprovoked seizure and a high risk of having another over the following years (similar to someone who has already had two);
• they have been diagnosed with a specific epilepsy syndrome.

How common is it?

Epilepsy is one of the most common neurological conditions. An analysis of more than 200 studies worldwide estimated that between 6 and 8 in every 1,000 people have or have had active epilepsy, with somewhat higher figures in low- and middle-income countries.2 It can begin at any age, from infancy to old age.

What happens in the brain during a seizure?

A good way to picture the brain is as a car with an accelerator and a brake. The accelerator is excitatory signaling (mainly the neurotransmitter glutamate), which pushes neurons to become active. The brake is inhibitory signaling (mainly the neurotransmitter GABA), which calms them down. In a healthy brain, the two stay in balance.

When that balance tips toward excitation, circuits become hyperexcitable: neurons are too ready to fire, and a small spark can spread and recruit many neurons at once. That is a seizure.

For the brake to work, GABA depends on something that is often overlooked: the amount of chloride inside neurons. Two membrane proteins control it. One, called KCC2, pumps chloride out of the neuron and keeps the brake strong. The other, NKCC1, brings it in. If NKCC1 works too hard, chloride builds up inside the neuron and GABA loses part of its ability to brake — it can even become excitatory.3 This mechanism is one of the main research topics in our lab.

Not all seizures are convulsions

Many people associate epilepsy with falling down and whole-body shaking, but that is only one of many possible forms. The ILAE distinguishes two broad groups:4

• Focal seizures, which start in one area of one hemisphere of the brain. The person may or may not stay aware. They can appear as a strange feeling, a smell or taste that isn't there, movements of one part of the body, or automatic actions such as chewing or rubbing the hands. Sometimes a focal seizure spreads and becomes bilateral.
• Generalized seizures, which involve both hemispheres from the start. They include tonic-clonic seizures (stiffening followed by jerking) and absence seizures, brief lapses of a few seconds that can go unnoticed or be mistaken for daydreaming.

What causes it?

The causes vary widely: genetic factors, brain injuries (for example, after a stroke, head trauma or infection), developmental malformations, and metabolic or immune disorders. In a substantial proportion of people, no cause is found.2 Epilepsy is not a mental illness, it is not contagious, and it says nothing about a person's intelligence.

Can it be treated?

Yes. The main treatment is antiseizure medication (formerly called antiepileptic drugs). In a 30-year follow-up of almost 1,800 people, about two in three achieved seizure control, most of them with the first or second medication they tried. However, a little over one third kept having seizures despite treatment — a proportion that has not changed much even as new drugs have become available.5 For these people there are other options, such as epilepsy surgery, nerve stimulation or special diets, which should be evaluated by a specialized team.

That third of people with hard-to-control epilepsy is one of the reasons we keep studying the basic mechanisms of hyperexcitability: understanding them better can open the way to new treatments.

What we study

In our lab we use animal models to study how changes in chloride handling weaken inhibition in the hippocampus, a brain region frequently involved in temporal lobe epilepsy. You can read more on our epilepsy research page, or explore interactively how a seizure starts and spreads in our simulators.

References

1. Fisher RS, et al. ILAE official report: a practical clinical definition of epilepsy. Epilepsia. 2014;55(4):475–482. doi:10.1111/epi.12550
2. Fiest KM, et al. Prevalence and incidence of epilepsy: a systematic review and meta-analysis of international studies. Neurology. 2017;88(3):296–303. doi:10.1212/WNL.0000000000003509
3. Kaila K, Price TJ, Payne JA, Puskarjov M, Voipio J. Cation-chloride cotransporters in neuronal development, plasticity and disease. Nat Rev Neurosci. 2014;15(10):637–654. doi:10.1038/nrn3819
4. Fisher RS, et al. Operational classification of seizure types by the International League Against Epilepsy. Epilepsia. 2017;58(4):522–530. doi:10.1111/epi.13670
5. Chen Z, Brodie MJ, Liew D, Kwan P. Treatment outcomes in patients with newly diagnosed epilepsy treated with established and new antiepileptic drugs: a 30-year longitudinal cohort study. JAMA Neurol. 2018;75(3):279–286. doi:10.1001/jamaneurol.2017.3949

This text is for educational purposes and does not replace assessment by a health professional. If you or someone close to you has had a seizure, see a doctor or neurologist.