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Moreover, seizures are a frequent symptom in demyelinating diseases, such as multiple sclerosis, and in animal models of demyelination and oligodendrocyte dysfunction. Finally, the excessive activity reported in demyelinated axons may promote hyperexcitability. We hypothesize that the extracellular potassium rise generated during epileptiform activity may be amplified by the presence of axons without appropriate myelin coating and by alterations in oligodendrocyte function. This process could facilitate the triggering of recurrent spontaneous seizures in areas of altered myelination and could result in further demyelination, thus promoting epileptogenesis.<\/jats:p>","DOI":"10.1111\/epi.16824","type":"journal-article","created":{"date-parts":[[2021,1,25]],"date-time":"2021-01-25T22:31:23Z","timestamp":1611613883000},"page":"583-595","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":58,"title":["A hypothesis for the role of axon demyelination in seizure generation"],"prefix":"10.1111","volume":"62","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-7443-6737","authenticated-orcid":false,"given":"Marco","family":"de Curtis","sequence":"first","affiliation":[{"name":"Epilepsy Unit IRCCS Foundation Carlo Besta Neurological Institute Milan 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