Editing Epilepsy (section)

=== Seizures ===
In a healthy brain, neurons communicate through electrical signals that are generally desynchronized. This activity is tightly regulated by a balance between excitatory and inhibitory influences. Intracellular factors that influence neuronal excitability include the type, number, and distribution of [[Ion channel|ion channels]], as well as alterations in [[Receptor (biochemistry)|receptor]] function and [[gene expression]]. Extracellular factors include ionic concentrations in the surrounding environment, [[synaptic plasticity]], and the regulation of neurotransmitter breakdown by [[Neuroglia|glial cells]].<ref>{{cite journal |vauthors=Blumenfeld H |year=2005 |title=Cellular and network mechanisms of spike-wave seizures |journal=Epilepsia |volume=46 |issue=Suppl.9 |pages=21–33 |doi=10.1111/j.1528-1167.2005.00311.x |pmid=16302873 |doi-access=free}}</ref><ref name="Intro2006">{{cite book |url=https://www.ncbi.nlm.nih.gov/books/NBK2510/ |title=An Introduction to Epilepsy |vauthors=Bromfield EB |publisher=American Epilepsy Society |year=2006 |chapter=Basic Mechanisms Underlying Seizures and Epilepsy}}</ref>

During a seizure, this balance breaks down, leading to a sudden and excessive synchronization of neuronal firing. A localized group of neurons may begin firing together in an abnormal and repetitive pattern, overwhelming normal inhibitory controls. This abnormal activity can remain confined to a specific region of the brain or propagate to other areas. The process by which this transition occurs is known as [[ictogenesis]]. It involves a shift in network dynamics, typically beginning with excessive excitatory activity in a susceptible area of cortex — known as a seizure focus — and failure of inhibitory mechanisms to contain it. At the cellular level, ictogenesis is often marked by a [[paroxysmal depolarizing shift]], a characteristic pattern of sustained neuronal depolarization followed by rapid repetitive firing.<ref>{{cite book |url=https://books.google.com/books?id=WjSoQVt-taYC&pg=PA167 |title=Ions in the Brain Normal Function, Seizures, and Stroke. |vauthors=Somjen GG |publisher=Oxford University Press |year=2004 |isbn=978-0-19-803459-9 |location=New York |page=167}}</ref> As excitatory feedback loops engage and inhibition further declines, the seizure may become self-sustaining and spread to other regions of the brain.<ref name="Epi2008p483">{{cite book |url=https://books.google.com/books?id=TwlXrOBkAS8C&pg=PA483 |title=Epilepsy: a comprehensive textbook |publisher=Wolters Kluwer Health/Lippincott Williams & Wilkins |year=2008 |isbn=978-0-7817-5777-5 |veditors=Engel J, Pedley TA |edition=2nd |location=Philadelphia |page=483}}</ref>

There is evidence that epileptic seizures are usually not a random event. Seizures are often brought on by factors (also known as triggers) such as stress, [[Alcohol use disorder|excessive alcohol use]], flickering light, or a lack of sleep, among others. The term [[seizure threshold]] is used to indicate the amount of [[Stimulus (physiology)|stimulus]] necessary to bring about a seizure; this threshold is lowered in epilepsy.<ref name="quyen2003">{{cite journal |vauthors=Le Van Quyen M, Navarro V, Martinerie J, Baulac M, Varela FJ |year=2003 |title=Toward a neurodynamical understanding of ictogenesis |journal=Epilepsia |volume=44 |issue=Suppl.12 |pages=30–43 |doi=10.1111/j.0013-9580.2003.12007.x |pmid=14641559 |doi-access=free}}</ref> The seizures can be described on different scales, from the cellular level<ref name="pmid35031915">{{cite journal |vauthors=Depannemaecker D, Ivanov A, Lillo D, Spek L, Bernard C, Jirsa V |date=February 2022 |title=A unified physiological framework of transitions between seizures, sustained ictal activity and depolarization block at the single neuron level |journal=Journal of Computational Neuroscience |volume=50 |issue=1 |pages=33–49 |doi=10.1007/s10827-022-00811-1 |pmc=8818009 |pmid=35031915}}</ref> to the whole brain.<ref>{{cite journal |vauthors=Depannemaecker D, Destexhe A, Jirsa V, Bernard C |date=August 2021 |title=Modeling seizures: From single neurons to networks |journal=Seizure |volume=90 |pages=4–8 |doi=10.1016/j.seizure.2021.06.015 |pmid=34219016 |doi-access=free}}</ref>