{"title":"与流感相关的脑病","authors":"Andrew Silverman, Chrisoula Cheronis","doi":"10.1002/cns3.70010","DOIUrl":null,"url":null,"abstract":"<p>This previously healthy and vaccinated (except for the seasonal influenza vaccine) 12-year-old boy developed acute neurological symptoms following 3 days of fever and gastrointestinal distress. His symptoms progressed from headache and transient left-arm paresthesias to expressive aphasia, prompting emergency evaluation. He was febrile, tachycardic, and hypertensive on arrival, with fluctuating neurological deficits. Serum investigations, including blood counts, glucose, metabolic panel, urine toxicology, and anti-MOG, were normal. Influenza B was detected via nasopharyngeal swab. Magnetic resonance imaging/magnetic resonance angiography revealed confluent white matter signal changes with restricted diffusion (Figure 1) with normal vessels, consistent with an infection-triggered encephalopathy syndrome, specifically mild encephalopathy with a reversible splenial lesion (MERS) [<span>2</span>]. The patient's rapid clinical improvement within 24 h without treatment supported a diagnosis of influenza-associated encephalopathy (IAE), for which neuroimaging is paramount. Diffusion restriction was thought to be related to intramyelinic edema and/or inflammatory infiltrate, comparable to prior reports [<span>1, 3</span>]. At 3-month follow-up, he remained neurologically intact, had returned to age-appropriate schooling, and had normal repeat imaging. IAE is a rare but severe complication of influenza; the pathogenesis is not fully understood but is believed to involve dysregulated host inflammatory response to influenza, leading to varying degrees of brain dysfunction and inflammation [<span>4, 5</span>]. This patient with MERS with focal neurological deficits and extensive white matter involvement illustrates the variable presentation and rapid reversibility of IAE in some individuals. In contrast, more severe types of IAE require immediate neuroprotective measures in intensive care and prompt immunotherapy (namely, acute necrotizing encephalopathy) [<span>2, 6</span>]. Given the significant proportion of pediatric influenza-associated deaths involving IAE in the 2024-25 influenza season, prevention strategies, including seasonal influenza vaccination, remain critical [<span>7, 8</span>].</p><p><b>Andrew Silverman:</b> conceptualization, investigation, visualization, writing – review and editing, writing – original draft. <b>Chrisoula Cheronis:</b> conceptualization, visualization, writing – review and editing, writing – original draft, investigation.</p><p>The authors declare no conflicts of interest.</p>","PeriodicalId":72232,"journal":{"name":"Annals of the Child Neurology Society","volume":"3 3","pages":"247-248"},"PeriodicalIF":0.0000,"publicationDate":"2025-06-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/cns3.70010","citationCount":"0","resultStr":"{\"title\":\"Influenza-Associated Encephalopathy\",\"authors\":\"Andrew Silverman, Chrisoula Cheronis\",\"doi\":\"10.1002/cns3.70010\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p>This previously healthy and vaccinated (except for the seasonal influenza vaccine) 12-year-old boy developed acute neurological symptoms following 3 days of fever and gastrointestinal distress. His symptoms progressed from headache and transient left-arm paresthesias to expressive aphasia, prompting emergency evaluation. He was febrile, tachycardic, and hypertensive on arrival, with fluctuating neurological deficits. Serum investigations, including blood counts, glucose, metabolic panel, urine toxicology, and anti-MOG, were normal. Influenza B was detected via nasopharyngeal swab. Magnetic resonance imaging/magnetic resonance angiography revealed confluent white matter signal changes with restricted diffusion (Figure 1) with normal vessels, consistent with an infection-triggered encephalopathy syndrome, specifically mild encephalopathy with a reversible splenial lesion (MERS) [<span>2</span>]. The patient's rapid clinical improvement within 24 h without treatment supported a diagnosis of influenza-associated encephalopathy (IAE), for which neuroimaging is paramount. Diffusion restriction was thought to be related to intramyelinic edema and/or inflammatory infiltrate, comparable to prior reports [<span>1, 3</span>]. At 3-month follow-up, he remained neurologically intact, had returned to age-appropriate schooling, and had normal repeat imaging. IAE is a rare but severe complication of influenza; the pathogenesis is not fully understood but is believed to involve dysregulated host inflammatory response to influenza, leading to varying degrees of brain dysfunction and inflammation [<span>4, 5</span>]. This patient with MERS with focal neurological deficits and extensive white matter involvement illustrates the variable presentation and rapid reversibility of IAE in some individuals. In contrast, more severe types of IAE require immediate neuroprotective measures in intensive care and prompt immunotherapy (namely, acute necrotizing encephalopathy) [<span>2, 6</span>]. Given the significant proportion of pediatric influenza-associated deaths involving IAE in the 2024-25 influenza season, prevention strategies, including seasonal influenza vaccination, remain critical [<span>7, 8</span>].</p><p><b>Andrew Silverman:</b> conceptualization, investigation, visualization, writing – review and editing, writing – original draft. <b>Chrisoula Cheronis:</b> conceptualization, visualization, writing – review and editing, writing – original draft, investigation.</p><p>The authors declare no conflicts of interest.</p>\",\"PeriodicalId\":72232,\"journal\":{\"name\":\"Annals of the Child Neurology Society\",\"volume\":\"3 3\",\"pages\":\"247-248\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2025-06-17\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://onlinelibrary.wiley.com/doi/epdf/10.1002/cns3.70010\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Annals of the Child Neurology Society\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://onlinelibrary.wiley.com/doi/10.1002/cns3.70010\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Annals of the Child Neurology Society","FirstCategoryId":"1085","ListUrlMain":"https://onlinelibrary.wiley.com/doi/10.1002/cns3.70010","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
This previously healthy and vaccinated (except for the seasonal influenza vaccine) 12-year-old boy developed acute neurological symptoms following 3 days of fever and gastrointestinal distress. His symptoms progressed from headache and transient left-arm paresthesias to expressive aphasia, prompting emergency evaluation. He was febrile, tachycardic, and hypertensive on arrival, with fluctuating neurological deficits. Serum investigations, including blood counts, glucose, metabolic panel, urine toxicology, and anti-MOG, were normal. Influenza B was detected via nasopharyngeal swab. Magnetic resonance imaging/magnetic resonance angiography revealed confluent white matter signal changes with restricted diffusion (Figure 1) with normal vessels, consistent with an infection-triggered encephalopathy syndrome, specifically mild encephalopathy with a reversible splenial lesion (MERS) [2]. The patient's rapid clinical improvement within 24 h without treatment supported a diagnosis of influenza-associated encephalopathy (IAE), for which neuroimaging is paramount. Diffusion restriction was thought to be related to intramyelinic edema and/or inflammatory infiltrate, comparable to prior reports [1, 3]. At 3-month follow-up, he remained neurologically intact, had returned to age-appropriate schooling, and had normal repeat imaging. IAE is a rare but severe complication of influenza; the pathogenesis is not fully understood but is believed to involve dysregulated host inflammatory response to influenza, leading to varying degrees of brain dysfunction and inflammation [4, 5]. This patient with MERS with focal neurological deficits and extensive white matter involvement illustrates the variable presentation and rapid reversibility of IAE in some individuals. In contrast, more severe types of IAE require immediate neuroprotective measures in intensive care and prompt immunotherapy (namely, acute necrotizing encephalopathy) [2, 6]. Given the significant proportion of pediatric influenza-associated deaths involving IAE in the 2024-25 influenza season, prevention strategies, including seasonal influenza vaccination, remain critical [7, 8].
Andrew Silverman: conceptualization, investigation, visualization, writing – review and editing, writing – original draft. Chrisoula Cheronis: conceptualization, visualization, writing – review and editing, writing – original draft, investigation.