{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,5]],"date-time":"2026-08-05T12:22:26Z","timestamp":1785932546937,"version":"3.56.0"},"reference-count":27,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2025,9,25]],"date-time":"2025-09-25T00:00:00Z","timestamp":1758758400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Immunol."],"abstract":"<jats:p>The COVID-19 pandemic has unveiled the pivotal role of systemic inflammatory responses in neurological complications, particularly parainfectious encephalopathy. Accumulating evidence has established innate immune overreaction\u2014distinct from direct viral neuro-invasion or autoantibody-mediated reaction\u2014as the fundamental mechanism. The clinical manifestations of parainfectious encephalopathy are highly diverse, spanning from mild cases, such as mild encephalopathy with or without a reversible splenial lesion (MERS or ME), to catastrophic syndromes like acute necrotizing encephalopathy (ANE) and febrile infection-related epilepsy syndrome with or without a claustrum lesion (FIRES-C or FIRES). In this article, we summarize the phenotypes, diagnosis, and treatment strategies for parainfectious encephalopathy to enhance clinical recognition and understanding of this re-emerging disorder.<\/jats:p>","DOI":"10.3389\/fimmu.2025.1634383","type":"journal-article","created":{"date-parts":[[2025,9,25]],"date-time":"2025-09-25T04:17:30Z","timestamp":1758773850000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":1,"title":["Rediscovering parainfectious encephalopathy in the post-COVID-19 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