Editing Epilepsy (section)

=== Epilepsy ===
While ictogenesis explains how individual seizures arise, it does not account for why the brain develops a persistent tendency to generate them. This longer-term process is known as [[epileptogenesis]] — the sequence of biological events that transforms a previously non-epileptic brain into one capable of producing spontaneous seizures. It can occur after a wide range of brain insults, including traumatic brain injury, stroke, central nervous system infections, brain tumors, or prolonged seizures (such as [[status epilepticus]]). In most cases, no clear cause is identified. Although not fully understood, it involves a range of biological changes, including neuronal loss, synaptic reorganization, gliosis, neuroinflammation, and disruption of the blood–brain barrier.<ref name="Pitkänen2014" /><ref name="Noebels2014">{{cite book |url=https://books.google.com/books?id=T2_LVTB7ftgC&pg=466 |title=Jasper's Basic Mechanisms of the Epilepsies |vauthors=Noebels JL, Avoli M |date=29 June 2012 |publisher=Oxford University Press |isbn=978-0-19-974654-5 |pages=466, 470 |access-date=16 October 2014}}</ref>

Together, these changes contribute to the formation of hyperexcitable neural networks, often anchored around a seizure focus. Once established, this pathological network increases the brain's susceptibility to seizures, even in the absence of ongoing injury. Although many of the processes underlying ictogenesis and epileptogenesis have been identified, the exact mechanisms by which the brain transitions into a seizure or becomes epileptic remain unknown.<ref name="Noebels2014" /> Research continues to explore how genetic, molecular, and network-level factors interact to produce the diverse manifestations of epilepsy.