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Epileptogenesis is the process by which the brain develops epilepsy, often divided into:
Acute injury, a latent period (lasting months or sometimes years) and spontaneous seizures.

Multiple disease mechanisms underpinned by genetic mutations have been implicated in the development of epilepsy. Variation in phenotype of genetic epilepsy can be driven by changes at the gene level, within the neuron, or across networks of neurons.

Inflammation is now viewed by some as an intrinsic part of some forms of epilepsy, being the cause of, as well as the result of, a seizure.

In epilepsy, many of the cells that support normal neural functioning become reactive or
pro-inflammatory, including microglia, and astrocytes.

The blood–brain barrier is often dysregulated in epilepsy, and as a result, much research has focused on whether this is a cause or a result of seizures, or potentially both.

Blood–brain barrier (BBB) breakdown in epilepsy drives seizure susceptibility in a positive feedback loop, and is seen by some as a biomarker of epileptogenesis.