{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,24]],"date-time":"2026-09-24T08:12:02Z","timestamp":1790237522006,"version":"4.1.0"},"reference-count":57,"publisher":"Wiley","issue":"9","license":[{"start":{"date-parts":[[2023,7,25]],"date-time":"2023-07-25T00:00:00Z","timestamp":1690243200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Epilepsia"],"published-print":{"date-parts":[[2023,9]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    Seizures resulting from cerebral autoimmunity are either acutely symptomatic in the context of autoimmune encephalitis (AIE) with neural surface antibodies, or they are indicative of an enduring predisposition to seizures, that is, epilepsy. Here, we propose a practical definition for autoimmune encephalitis\u2010associated epilepsy (AEAE): Seizures associated with antibodies against glutamic acid decarboxylase, paraneoplastic syndromes, or Rasmussen encephalitis are classified as AEAE. AEAE secondary to AIE with antibodies against the\n                    <jats:italic>N<\/jats:italic>\n                    \u2010methyl\u2010D\u2010aspartate receptor, leucine\u2010rich glioma inactivated protein 1, contactin\u2010associated protein\u20102, or \u03b3\u2010aminobutyric acid\u2010B receptor can be diagnosed if the following criteria are met: seizures persist for at least 2\u2009years after immunotherapy initiation; no signs of encephalitis on magnetic resonance imaging and no fluorodeoxyglucose positron emission tomography hypermetabolism; normal cerebrospinal fluid cell count; and a substantial decrease in antibody titers. This classification corresponds to different disease mechanisms. While AIE results from the pathogenic effects of neural antibodies, AEAE is probably the consequence of encephalitis\u2010related tissue damage and thereby mainly structurally mediated. The distinction between AIE and AEAE also has practical consequences: In AIE, immunotherapy is usually highly beneficial, whereas anti\u2010seizure medication has little effect. In AEAE, immunotherapy is less promising and the usual anti\u2010seizure interventions are preferable. In addition, the diagnosis of AEAE has social consequences in terms of driving and professional limitations.\n                  <\/jats:p>","DOI":"10.1111\/epi.17699","type":"journal-article","created":{"date-parts":[[2023,6,24]],"date-time":"2023-06-24T21:20:19Z","timestamp":1687641619000},"page":"2249-2255","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":39,"title":["What is autoimmune encephalitis\u2010associated epilepsy? 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