Central nervous system (CNS) inflammatory demyelinating diseases (IDDs) associated with COVID-19: A case series and review

Feizi, Parissa; Sharma, K Aparna; Pasham, Shreya R.; Nirwan, Lalit; Joseph, Joe; Jaiswal, Shruti; Sriwastava, Shitiz

doi:10.1016/j.jneuroim.2022.577939

Cited by 18 publications

(25 citation statements)

References 66 publications

(101 reference statements)

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“…Another study has reported that 365 (22%) of 1,695 patients hospitalized with COVID-19 had documented neurologic involvement, among which 43 (12%) developed life-threatening conditions, including 15 with severe encephalopathy (LaRovere et al, 2021). In addition, at least 18 patients with acquired demyelinating syndromes were reported as neurological complications of COVID-19, of which NMOSD was the most common (n = 7) (Feizi et al, 2022). Some infection-triggered acute encephalopathies are characterized by a stereotypical clinical course and specific neuroimaging findings, and thus we recognized these as specific clinico-radiological syndromes and analyzed the cases of acute encephalopathy from this perspective (Mizuguchi et al, 2007).…”

Section: Discussionmentioning

confidence: 99%

Severe pediatric acute encephalopathy syndromes related to SARS-CoV-2

Sakuma

Takanashi²,

Muramatsu³

et al. 2023

Front. Neurosci.

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Background and objectivesTo clarify whether severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection cause acute encephalopathy in children and which are the most common syndromes that cause them and what are the outcomes.MethodsA nationwide web-based survey among all members of the Japanese Society of Child Neurology to identify pediatric patients aged < 18 years who developed acute encephalopathy in Japan between 1 January 2020 and 31 May 2022 associated with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection confirmed by polymerase chain reaction or antigen tests using pharyngeal swabs. Acute encephalopathy was defined as acute onset of impaired consciousness lasting > 24 h or an altered mental state; neurological symptoms arising within 2 weeks of onset of COVID-19 or multisystem inflammatory syndrome in children (MIS-C)/pediatric inflammatory multisystem syndrome (PIMS); evidence of SARS-CoV-2 infection; and reasonable exclusion of other diseases. Patients were divided into the known clinico-radiological acute encephalopathy syndrome group and unexplained or unclassifiable acute encephalopathy group. Outcomes were assessed by pediatric cerebral performance category (PCPC) score at hospital discharge.ResultsOf the 3,802 society members, 217 representing institutions responded, and 39 patients with suspected acute encephalopathy were reported, of which 31 met inclusion criteria. Of these patients, 14 were diagnosed with known clinico-radiological acute encephalopathy syndromes, with acute encephalopathy with biphasic seizures and late reduced diffusion (five patients) being the most common. Five developed acute encephalopathy associated with MIS-C/PIMS. Among 31 patients, 9 (29.0%) had severe sequelae or died (PCPC ≥ 4). Two of three patients with encephalopathy with acute fulminant cerebral edema and two with hemorrhagic shock and encephalopathy syndrome died. The PCPC scores were higher in the known clinico-radiological acute encephalopathy syndrome group than in the unexplained or unclassifiable acute encephalopathy group (P < 0.01).DiscussionAcute encephalopathy related to SARS-CoV-2 infection was demonstrated to be more severe than that caused by other viruses in Japan. Acute encephalopathy syndromes characterized by specific neuroradiological findings was associated with poor clinical outcomes.

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Section: Discussionmentioning

confidence: 99%

Severe pediatric acute encephalopathy syndromes related to SARS-CoV-2

Sakuma

Takanashi²,

Muramatsu³

et al. 2023

Front. Neurosci.

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“…The correlation of NMOSD after acute COVID-19 infection is not fully understood. A recent article reported seven NMOSD cases, six of which were aquaporin positive after COVID-19 infection [14]. Demyelinating changes may occur owing to a hyperinflammatory state with the release of cytokines caused by infection leading to glial activation, or it may occur as part of a delayed immune response [15].…”

Section: Discussionmentioning

confidence: 99%

Multiple Sclerosis and Neuromyelitis Optica Spectrum Disorder: Onset Following Acute COVID-19 Infection, a Case Series

et al. 2022

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Background and Objectives: Acute COVID-19 infection has been associated with neurological involvement. We report a case series of newly diagnosed patients with multiple sclerosis (MS) and neuromyelitis optica spectrum disorder (NMOSD) developed in a short period of time after acute COVID-19 infection. Methods: New MS patients developing initial symptoms shortly after an acute COVID-19 infection were diagnosed based on the 2017 McDonald Criteria [Garcia-Ramos et al. in Cells, 2021]. The patients diagnosed with NMOSD met the 2015 International Panel criteria for the diagnosis of NMOSD (IPDN) [Thompson et al. in Lancet Neurol 17:162-173, 2018]. Results From the MS Patient Group: Ten patients were included who had developed initial MS symptoms after COVID-19 infection. Gender distribution was equal (50% male). The mean age was 28 (range 17-39) years. Average time to neurological presentation was between 2 and 6 weeks following acute COVID-19 infection. Partial transverse myelitis was the initial presentation in 40% of the cases, and 60% of patients had spinal cord lesions present at the moment of diagnosis. All patients showed enhancing lesions on brain magnetic resonance imaging (MRI). The presence of cerebrospinal fluid (CSF) oligoclonal bands was found in all six tested cases. The majority of patients (80%) were unvaccinated for COVID-19. The two vaccinated patients had received two doses of the monovalent COVID-19 messenger ribonucleic acid (mRNA) (Pfizer Biotech) vaccine and no booster, a year prior to contracting COVID-19.Results From the NMOSD Group: Two patients with NMOSD were included. Positive aquoporin-4 protein antibody (AQP-4 Ab) was detected in serum in both cases [one Enzyme Linked immunosorbent assay (ELISA) and one cell based]. Both patients had mild COVID-19 infection prior to presentation, initial neurologic symptoms presented between 3 and 6 weeks after COVID-19 infection. Neither patients were vaccinated. Both responded partially to steroids, one developed a relapse 40 days after diagnosis. Conclusion: COVID-19 infection has been linked to several neurological and immune-driven conditions. This study suggests that in susceptible individuals, acute COVID-19 infection may act as a trigger for developing MS and NMOSD.

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“…Furthermore, recent findings do not indicate a significant increase in the incidence of MOGAD during the pandemic and MOGAD without COVID-19 occurs at the same frequency. 7 , 10 , 12 , 14 , 16 , 17 , 20 Moreover, MOGAD also occurs after vaccination with SARS-CoV-2 S mRNA or, in particular, vector vaccines. 8 , 9 , 11 , 13 , 15 , 18 , 19 , 21 All these reports are supported by our results in serological profiling of pre-pandemic and pandemic samples showing no or even negative correlation between the presence of MOG-IgG and antibodies to not only SARS-CoV-2 but also to CoV-229E, CoV-HKU1, CoV-OC43 and CoV-NL63.…”

Section: Discussionmentioning

confidence: 99%

Is there an immunological cross-reactivity of antibodies to the myelin oligodendrocyte glycoprotein and coronaviruses?

Schanda,

Mariotto,

Rudzki

et al. 2024

Brain Communications

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Recent reports indicated that myelin oligodendrocyte glycoprotein antibody-associated disease might be a rare complication after severe acute respiratory syndrome coronavirus 2 infection or vaccination. It is unclear whether this is an unspecific sequel of infection or vaccination or caused by possible immunological cross-reactivity of severe acute respiratory syndrome coronavirus 2 proteins and myelin oligodendrocyte glycoprotein. The aim of this study was therefore to elucidate whether there is an immunological cross-reactivity between severe acute respiratory syndrome coronavirus 2 spike or nucleocapsid proteins and myelin oligodendrocyte glycoprotein and to explore the relation of antibody responses against myelin oligodendrocyte glycoprotein and severe acute respiratory syndrome coronavirus 2 and other coronaviruses. We analysed serum samples from patients with severe acute respiratory syndrome coronavirus 2 infection and neurological symptoms with (myelin oligodendrocyte glycoprotein antibody-associated disease, n = 12) or without myelin oligodendrocyte glycoprotein-antibodies (n = 10); severe acute respiratory syndrome coronavirus 2 infection without neurological symptoms (n = 32); vaccinated patients with no history of severe acute respiratory syndrome coronavirus 2 infection and neurological symptoms with (myelin oligodendrocyte glycoprotein antibody-associated disease, n = 10) or without myelin oligodendrocyte glycoprotein-antibodies (n = 9); and severe acute respiratory syndrome coronavirus 2 negative/naïve unvaccinated patients with neurological symptoms with (myelin oligodendrocyte glycoprotein antibody-associated disease, n = 47) or without myelin oligodendrocyte glycoprotein-antibodies (n = 20). All samples were analysed for serum antibody responses to myelin oligodendrocyte glycoprotein, severe acute respiratory syndrome coronavirus 2, and other common coronaviruses (CoV-229E, CoV-HKU1, CoV-NL63 and CoV-OC43). Based on sample amount and antibody titres, 21 samples were selected for analysis of antibody cross-reactivity between myelin oligodendrocyte glycoprotein and severe acute respiratory syndrome coronavirus 2 spike and nucleocapsid proteins using affinity purification and pre-absorption. Whereas we found no association of immunoglobulin G and A myelin oligodendrocyte glycoprotein antibodies with coronavirus antibodies, infections with severe acute respiratory syndrome coronavirus 2 correlated with an increased immunoglobulin M myelin oligodendrocyte glycoprotein antibody response. Purified antibodies showed no cross-reactivity between severe acute respiratory syndrome coronavirus 2 spike protein and myelin oligodendrocyte glycoprotein. However, one sample of a patient with myelin oligodendrocyte glycoprotein antibody-associated disease following severe acute respiratory syndrome coronavirus 2 infection showed a clear immunoglobulin G antibody cross-reactivity to severe acute respiratory syndrome coronavirus 2 nucleocapsid protein and myelin oligodendrocyte glycoprotein. This patient was also seropositive for other coronaviruses and showed immunological cross-reactivity of severe acute respiratory syndrome coronavirus 2 and CoV-229E nucleocapsid proteins. Overall, our results indicate that an immunoglobulin G antibody cross-reactivity between myelin oligodendrocyte glycoprotein and severe acute respiratory syndrome coronavirus 2 proteins is rare. The presence of increased myelin oligodendrocyte glycoprotein-immunoglobulin M antibodies after severe acute respiratory syndrome coronavirus 2 infection may either be a consequence of a previous infection with other coronaviruses or arise as an unspecific sequel after viral infection. Furthermore, our data indicate that myelin oligodendrocyte glycoprotein-immunoglobulin A and particularly myelin oligodendrocyte glycoprotein-immunoglobulin M antibodies are a rather unspecific sequel of viral infections. Finally, our findings do not support a causative role of coronavirus infections for the presence of myelin oligodendrocyte glycoprotein-immunoglobulin G antibodies.

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Central nervous system (CNS) inflammatory demyelinating diseases (IDDs) associated with COVID-19: A case series and review

Cited by 18 publications

References 66 publications

Severe pediatric acute encephalopathy syndromes related to SARS-CoV-2

Severe pediatric acute encephalopathy syndromes related to SARS-CoV-2

Multiple Sclerosis and Neuromyelitis Optica Spectrum Disorder: Onset Following Acute COVID-19 Infection, a Case Series

Is there an immunological cross-reactivity of antibodies to the myelin oligodendrocyte glycoprotein and coronaviruses?

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