Neuroinflammatory Disease following Severe Acute Respiratory Syndrome Coronavirus 2 Infection in Children

Aubart, Mélodie; Roux, C.; Durrleman, C; Gins, Clarisse; Hully, M; Kossorotoff, Manoëlle; Gitiaux, C; Lévy, Raphaël; Moulin, F.; Debray, Agathe; Belhadjer, Zahra; Georget, Emilie; Tchameni, R Kom; Blanc, Pierluigi; Wehbi, S; Mazeghrane, M; Tencer, J; Gajdos, Vincent; Rouget, Sébastien; Pontual, Loïc de; Basmaci, Romain; Yacouben, K; Angoulvant, François; Leruez‐Ville, Marianne; Sterlin, D; Rozenberg, Felix D; Robert, Matthieu P.; Zhang, S Y; Boddaert, Nathalie; Desguerre, Isabelle

doi:10.1016/j.jpeds.2022.05.018

Cited by 18 publications

(41 citation statements)

References 33 publications

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“…In 10 case reports, AQP4-IgG Abs were positive ( 22 – 27 , 29 , 31 , 86 , 87 ). In two case reports the AQP4 abs were negative ( 30 , 32 ) and each fulfilled the diagnostic criteria for seronegative NMOSD.…”

Section: Resultsmentioning

confidence: 98%

“…One paper describes three patients with post-COVID-19 demyelinating events, of which one is NMOSD, one- MOGAD, and one- clinically isolated syndrome (CIS) ( 86 ). Another paper describes various CNS inflammatory diseases, of which three were MOGAD and one—NMOSD ( 87 ). A PRISMA flow chart illustrating the article selection process is presented in Figure 1 .…”

Section: Resultsmentioning

confidence: 99%

“…Collectively, 13 case reports and one case series describe the occurrence of 18 NMOSD-related clinical events in the context of COVID-19 ( 21 – 32 , 86 , 87 ). Eight patients were females, four were males, and in six cases the patients' sex was not reported.…”

Section: Resultsmentioning

confidence: 99%

“…Ten case reports describe the onset of newly diagnosed NMOSD in people without previous neurological disease ( 22 – 26 , 28 – 30 , 32 , 87 ). Two case reports describe people with previously undiagnosed neurological disease who then presented with a second clinical manifestation in temporal association to COVID-19, leading to an NMOSD diagnosis ( 27 , 86 ).…”

Section: Resultsmentioning

confidence: 99%

“…Treatment consisted of corticosteroid (CS) monotherapy in seven cases ( 21 , 22 , 28 , 87 ), CS + rituximab in two cases ( 26 , 32 ), intravenous methylprednisolone (IVMP)+ intravenous immunoglobulin (IVIG)+plasma exchange (PLEX) in one case ( 23 ), CS +IVIG+ rituximab in one case ( 30 ), and CS + PLEX in one case ( 25 ). In the remaining six cases, the treatment regimen was not reported ( 21 , 24 , 27 , 29 , 86 ).…”

Section: Resultsmentioning

confidence: 99%

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COVID-19 and the risk of CNS demyelinating diseases: A systematic review

et al. 2022

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BackgroundViral infections are a proposed possible cause of inflammatory central nervous system (CNS) demyelinating diseases, including multiple sclerosis (MS), neuromyelitis optica spectrum disorder (NMOSD), and myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD). During the past 2 years, CNS demyelinating events associated with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection have been reported, but causality is unclear.ObjectiveTo investigate the relationship between CNS demyelinating disease development and exacerbation with antecedent and/or concurrent SARS-CoV-2 infection.MethodsA systematic literature review of all publications describing either a new diagnosis or relapse of CNS demyelinating diseases (MS, NMOSD, MOGAD) in association with SARS-CoV-2 infection was performed utilizing PRISMA guidelines. Descriptive statistics were used for data analysis, using a case analysis approach.ResultsSixty-seven articles met the inclusion criteria for the study. Most of the reported cases of NMOSD (n = 13, 72.2% of reported cases) and MOGAD (n = 27, 96.5% of reported cases) were of new disease onset, presenting with typical clinical and radiographic features of these conditions, respectively. In contrast, reported MS cases varied amongst newly diagnosed cases (n = 10, 10.5% of reported cases), relapses (n = 63, 66.4%) and pseudo-relapses (n = 22, 23.2%). The median duration between COVID-19 infection and demyelinating event onset was 11.5 days (range 0–90 days) in NMOSD, 6 days (range−7 to +45 days) in MOGAD, and 13.5 days (range−21 to +180 days) in MS. Most cases received high-dose corticosteroids with a good clinical outcome.ConclusionBased upon available literature, the rate of CNS demyelinating events occurring in the setting of preceding or concurrent SARS-CoV-2 infection is relatively low considering the prevalence of SARS-CoV-2 infection. The clinical outcomes of new onset or relapsing MS, NMOSD, or MOGAD associated with antecedent or concurrent infection were mostly favorable. Larger prospective epidemiological studies are needed to better delineate the impact of COVID-19 on CNS demyelinating diseases.

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Section: Resultsmentioning

confidence: 98%

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

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COVID-19 and the risk of CNS demyelinating diseases: A systematic review

et al. 2022

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Overview of autoantibodies in COVID‐19 convalescents

Dobrowolska

Zarębska-Michaluk

Siller‐Matula

et al. 2023

Journal of Medical Virology

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Accumulating evidence shows that SARS‐CoV‐2 can potentially trigger autoimmune processes, which can be responsible for the long‐term consequences of COVID‐19. Therefore, this paper aims to review the autoantibodies reported in COVID‐19 convalescents. Six main groups were distinguished: (i) autoantibodies against components of the immune system, (ii) autoantibodies against components of the cardiovascular system, (iii) thyroid autoantibodies, (iv) autoantibodies specific for rheumatoid diseases, (v) antibodies against G‐protein coupled receptors, and (vi) other autoantibodies. The evidence reviewed here clearly highlights that SARS‐CoV‐2 infection may induce humoral autoimmune responses. However, the available studies share number of limitations, such as: (1) the sole presence of autoantibodies does not necessarily implicate the clinically‐relevant risks, (2) functional investigations were rarely performed and it is often unknown whether observed autoantibodies are pathogenic, (3) the control seroprevalence, in healthy, noninfected individuals was often not reported; thus it is sometimes unknown whether the detected autoantibodies are the result of SARS‐CoV‐2 infection or the accidental post‐COVID‐19 detection, (4) the presence of autoantibodies was rarely correlated with symptoms of the post‐COVID‐19 syndrome, (5) the size of the studied groups were often small, (6) the studies focused predominantly on adult populations, (7) age‐ and sex‐related differences in seroprevalence of autoantibodies were rarely explored, (8) genetic predispositions that may be involved in generation of autoantibodies during SARS‐CoV‐2 infections were not investigated, and (9) the autoimmune reactions following infection with SARS‐CoV‐2 variants that vary in the clinical course of infection remain unexplored. Further longitudinal studies are advocated to assess the link between identified autoantibodies and particular clinical outcomes in COVID‐19 convalescents.

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Infection and inflammation: radiological insights into patterns of pediatric immune-mediated CNS injury

Malik

Shroff

2022

Neuroradiology

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The central nervous system (CNS) undergoes constant immune surveillance enabled via regionally specialized mechanisms. These include selectively permissive barriers and modifications to interlinked innate and adaptive immune systems that detect and remove an inciting trigger. The end-points of brain injury and edema from these triggers are varied but often follow recognizable patterns due to shared underlying immune drivers. Imaging provides insights to understanding these patterns that often arise from unique interplays of infection, inflammation and genetics. We review the current updates in our understanding of these intersections and through examples of cases from our practice, highlight that infection and inflammation follow diverse yet convergent mechanisms that can challenge the CNS in children. Supplementary Information The online version contains supplementary material available at 10.1007/s00234-022-03100-x.

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Neuroinflammatory Disease following Severe Acute Respiratory Syndrome Coronavirus 2 Infection in Children

Cited by 18 publications

References 33 publications

COVID-19 and the risk of CNS demyelinating diseases: A systematic review

COVID-19 and the risk of CNS demyelinating diseases: A systematic review

Overview of autoantibodies in COVID‐19 convalescents

Infection and inflammation: radiological insights into patterns of pediatric immune-mediated CNS injury

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