In the basic science realm you often hear epilepsy researchers refer to the "seizure threshold". Experimentally, this refers to the minimum stimulation required to trigger a seizure, be it an electrical stimulation, a chemical compound that stimulates the brain, an external stimulus such as a strobe light or noise, etc.
Every brain has a seizure threshold. Everyone can have a seizure if their brain is over-stimulated. Students have been reported to have "exam seizures". These are seizures as a result of lack of sleep, too much caffeine (or other drugs), high stress, etc.
Individuals with epilepsy, however, are thought to have chronically low seizure thresholds (i.e., their brains are more susceptible to being stimulated above their seizure threshold). I've made this simple illustration to show the concept of seizure threshold.
Anticonvulsant treatments ( drugs, ketogenic diet, etc.) are thought to elevate the seizure threshold. The GABA drugs [e.g., phenobarbital* (Luminal®), primidone (Mysoline®), topiramate (Topamax®), diazepam (Valium®), tiagabine (Gabitril®), vigabatrin (Sabril®), clonazepam (Rivatril®)] raise brain levels of the inhibitory chemical GABA. This makes the brain less excitable. The sodium channel drugs [phenytoin (Dilantin®), carbamazepine* (Tegretol®), felbamate (Felbatol®), lamotrigine (Lamictal®), levetiracetam (Keppra®), pregabalin (Lyrica®), topiramate (Topamax®) and zonisamide (Zonegran®)] make neurons fire more slowly, therefore making the brain less prone to seizures. The ketogenic diet also makes the brain less excitable, although the mechanisms (i.e., "how) are less clear.
The concept of seizure threshold helps us understand both "why" and "how" the brain enters a seizure. Better understanding of what causes the seizure threshold to change may help us understand why the brain enters into a seizure.