Editing Seizure (section)

== Mechanism ==
Seizures are the result of abnormal, excessive, and hypersynchronous neuronal activity in the brain. At a cellular level, they reflect a disruption of the normal balance between excitatory and inhibitory neurotransmission. Under healthy conditions, excitatory neurotransmission (mainly mediated by [[glutamate]]) and inhibitory neurotransmission (primarily via [[GABA]]) maintain cortical stability. An excess of excitation or a failure of inhibition can tip this balance, promoting hypersynchronous neuronal firing characteristic of seizures.<ref name="Tatti2016">{{Cite journal |last1=Tatti |first1=Roberta |last2=Haley |first2=Melissa S. |last3=Swanson |first3=Olivia K. |last4=Tselha |first4=Tenzin |last5=Maffei |first5=Arianna |date=2017-05-15 |title=Neurophysiology and Regulation of the Balance Between Excitation and Inhibition in Neocortical Circuits |journal=Biological Psychiatry |volume=81 |issue=10 |pages=821–831 |doi=10.1016/j.biopsych.2016.09.017 |issn=1873-2402 |pmc=5374043 |pmid=27865453}}</ref><ref name="Sarlo2021">{{Cite journal |last1=Sarlo |first1=Gabrielle L. |last2=Holton |first2=Kathleen F. |year=2021 |title=Brain concentrations of glutamate and GABA in human epilepsy: A review |url=https://linkinghub.elsevier.com/retrieve/pii/S1059131121002168 |journal=Seizure - European Journal of Epilepsy |language=en |volume=91 |pages=213–227 |doi=10.1016/j.seizure.2021.06.028 |pmid=34233236 |via=Elsevier Science Direct}}</ref><ref name="Treiman2001">{{Cite journal |last=Treiman |first=David M. |title=GABAergic Mechanisms in Epilepsy |url=https://onlinelibrary.wiley.com/doi/10.1046/j.1528-1157.2001.042suppl.3008.x |journal=Epilepsia |language=en |publication-date=2001 |volume=42 |issue=s3 |pages=8–12 |doi=10.1046/j.1528-1157.2001.042suppl.3008.x |issn=0013-9580 |pmid=11520315 |via=Wiley Online Library}}</ref> The generation of a seizure—the transition from an interictal to an ictal state—is known as [[ictogenesis]]. This process involves a cascade of physiological and network-level changes that lead to the sudden onset of pathological activity.

In provoked seizures (e.g., due to trauma, metabolic insults, or infections), acute disturbances in ionic gradients, neurotransmitter release, and neuronal membrane stability may transiently lower the threshold for seizure activity.

Brief seizures, such as absence seizures lasting 5–10 seconds, do not cause observable brain damage.<ref name="Dingledine2014">{{Citation |last1=Dingledine |first1=Ray |title=When and How Do Seizures Kill Neurons, and Is Cell Death Relevant to Epileptogenesis? |date=2014 |work=Issues in Clinical Epileptology: A View from the Bench |volume=813 |pages=109–122 |editor-last=Scharfman |editor-first=Helen E. |place=Dordrecht |publisher=Springer Netherlands |language=en |doi=10.1007/978-94-017-8914-1_9 |isbn=978-94-017-8913-4 |pmc=4624106 |pmid=25012371 |last2=Varvel |first2=Nicholas H. |last3=Dudek |first3=F. Edward |editor2-last=Buckmaster |editor2-first=Paul S.}}</ref> More prolonged seizures have a higher risk of neuronal death.<ref name="Dingledine2014" />  Prolonged and recurrent seizures, such as status epilepticus, typically cause brain damage.<ref name="Dingledine2014" />  Scarring of brain tissue ([[gliosis]]), neuronal death, and shrinking of areas of the brain ([[atrophy]]) are linked to recurrent seizures.<ref name="Dingledine2014" /><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 |editor1=Jerome Engel Jr. |edition=2nd |location=Philadelphia |page=483 |editor2=Timothy A. Pedley}}</ref> These changes may lead to the development of epilepsy, in a process called [[epileptogenesis]].<ref name="Epi2008p483" />