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Background and aims: Objective: Several preclinical and clinical investigations have argued for nervous system involvement in SARS-CoV-2 infection. No data about clinical, imaging and biomarkers presentations as well as long-term outcomes are available for SARS-CoV-2 encephalitis in comparison with infectious and autoimmune encephalitis. Methods: The ENCOVID European registry included patients with probable or definite diagnosis of encephalitis with and without SARS-CoV-2 infection admitted for hospitalization in the European recruiting centers between February 1st 2020 and March 30th, 2021. Each patient underwent a standardized assessment including full infectious screening, CSF, EEG, MRI data. Clinical presentation and laboratory markers, severity of COVID-19 disease, response to treatment and outcomes were recorded. Results: Results – Out of 155 cases screened, forty-five cases of encephalitis positive for SARS-CoV-2 infection and 63 without COVID-19 with full available data were included. SARS-CoV-2 encephalitis exhibited common presentation with aphasia and dysarthria compared to non-COVID- encephalitis and exhibited higher prevalence of patients with normal MRI but mild hyperproteinorracchia/pleocytosis. Most SARS-CoV-2 cases appeared during the onset of COVID-19 and exhibited different response to treatment and long-term outcomes compared to non COVID encephalitis. Conclusions: Conclusions –The registry identified a wide spectrum of encephalitis associated with COVID19 infection, with clinical characteristics and course different from classical infectious and autoimmune encephalitis. Biomarkers studies are warranted in order to evaluate the specific inflammatory pathways associated with SARS-Cov-2 encephalitis.
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Objective: In this study we aimed to analyse if viral particles or pro-inflammatory mediators may cause neurological symptoms of SARS-CoV-2 infection. Background: Coronavirus disease (COVID-19) has been associated with a large variety of neurological disorders. However the mechanisms underlying these neurological complications remain elusive. Design/Methods: We checked for SARS-CoV-2 mRNA by qPCR, SARS-CoV-2-specific antibodies and for 49 cytokines/chemokines/growth factors (by Luminex) in the cerebrospinal fluid (CSF) +/-serum of a cohort of 17 COVID-19 patients with neurological presentation and 55 neurological controls (inflammatory, non inflammatory, multiple sclerosis). Results: We found SARS-CoV-2 mRNA and antibodies specific for this virus in the CSF of 0/17 and 8/16 COVID-19 patients, respectively. The presence of SARS-CoV-2 antibodies was explained by a rupture of the blood brain barrier (passive transfer) in 6/16 (37,5%), but an intrathecal synthesis of SARS-CoV2-specific antibodies was present in 2/17. As compared to SARS-CoV-2-negative NIND patients, the CSF of IND patients exhibited the highest level of chemokines (CCL4, CCL5, CXCL8, CXCL10, CXCL12, and CXCL13), followed the CSF of MS patients (CXCL12, and CXCL13). There was no difference between COVID-19 patients with neurological diseases compared to NIND even if some chemokines (CCL4, CCL5, CXCL8, andCXCL10) tended to be higher than NIND. Interestingly, among COVD-19 patients, the CSF of those with a severe disease (encephalitis/encephalopathy) contained higher levels CXCL8 and CXCL10 than those with other neurological presentations. Conclusions: Our results confirm the absence of obvious SARS-CoV-2 infection of the central nervous system and point to a mild inflammatory reaction reflecting an astrocytic reaction.
ABSTRACT
Background and aims: Coronavirus disease (COVID-19) has been associated with a large variety of neurological disorders. However the mechanisms underlying these neurological complications remain elusive. In this study we aimed at determining whether neurological symptoms were caused by SARS-CoV-2 direct infection of by proinflammatory mediators. Methods: We checked for SARS-CoV-2 RNA by RT-qPCR, SARS-CoV-2-specific antibodies and for 48 cytokines/ chemokines/growth factors (by Luminex) in the cerebrospinal fluids (CSF) ± sera of a cohort of 17 COVID- 19 patients with neurological presentation and 55 neurological control patients (inflammatory [IND], non inflammatory [NIND], multiple sclerosis [MS]). Results: We found SARS-CoV-2 RNA and antibodies specific for this virus in the CSF of 0/17 and 8/16 COVID- 19 patients, respectively. The presence of SARS-CoV-2 antibodies was explained by a rupture of the blood brain barrier (passive transfer) in 6/16 (38%). An intrathecal synthesis of SARS-CoV2-specific antibodies was present in 2/16 patients. Of the four categories of tested patients, the CSF of IND exhibited the highest level of chemokines (CCL4, CCL5, CXCL8, CXCL10, CXCL12, and CXCL13), followed by the CSF of MS patients (CXCL12, and CXCL13). There was no significant difference between COVID-19 and NIND patients, even if some chemokines (CCL4, CCL5, CXCL8, andCXCL10) tended to be higher in the former. Interestingly, among COVD-19 patients, the CSF of those with a severe disease (encephalitis/ encephalopathy) contained higher levels CXCL8 and CXCL10 than those with other neurological presentations. Conclusion: Our results do not show obvious SARS-CoV-2 infection of the central nervous system, but point to a mild inflammatory reaction reflecting an astrocytic reaction.
ABSTRACT
Various neuromuscular complications have been described in SARS-CoV-2 infection, especially Guillain-Barre syndrome (GBS) and Critical Illness neuromyopathy (CI-NM). Two representative cases are discussed below. It appears that GBS shares most of the characteristics of classical post-infectious GBS, but SARS-CoV-2 may contribute to the increased incidence of CI-NM. Other rare complications have been described, including Tapia Syndrome and Kawasaki-like multiple system inflammatory syndrome. The question of vaccination and the risk of immune-mediated neuropathies remains open, but the lack of reported cases is reassuring as these complications usually occur within 6 weeks after vaccination.
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BACKGROUND AND PURPOSE: The spectrum of COVID-19, caused by severe acute respiratory syndrome coronavirus 2 infection (SARS-CoV-2), includes different neurologic manifestations of the central and peripheral nervous system. METHODS: From March through April 2020, in two university hospitals located in western Switzerland, we examined three patients with Guillain-Barré syndrome (GBS) following SARS-CoV-2. RESULTS: These cases were characterized by a primary demyelinating electrophysiological pattern (Acute inflammatory demyelinating polyneuropathy or AIDP) and a less severe disease course compared to recently published case series. Clinical improvement was observed in all patients at week five. One patient was discharged from hospital after full recovery with persistence of minor neurological signs (areflexia). Two of the three patients remained hospitalized: one was able to walk and the other could stand up with assistance. CONCLUSIONS: We report three cases of typical GBS (AIDP) occurring after SARS-CoV-2 infection and presenting with a favourable clinical course. Given the interval between COVID-19-related symptoms and neurological manifestations (mean of 15 days) we postulate a secondary immune-mediated mechanism rather than direct viral damage.
Subject(s)
COVID-19/complications , Guillain-Barre Syndrome/etiology , Neural Conduction/physiology , Disease Progression , Female , Guillain-Barre Syndrome/drug therapy , Guillain-Barre Syndrome/physiopathology , Humans , Immunoglobulins, Intravenous/therapeutic use , Middle Aged , Switzerland , Treatment OutcomeABSTRACT
BACKGROUND AND PURPOSE: We systematically reviewed available evidence for reports of neurological signs and symptoms in patients with COVID-19 to identify cases with severe acute respiratory syndrome coronavirus (SARS-CoV)-2 infection or immune-mediated reaction in the nervous system. METHODS: We followed PRISMA guidelines and used the MEDLINE, EMBASE, Google Scholar, MedRxiv and ChinaXiv databases to search for articles on COVID-19 and nervous system involvement that were published from 1 January to 24 April 2020. Data on design, sample size, neurological assessment and related work-up were extracted. Biases were assessed with the Newcastle-Ottawa scale. RESULTS: We analysed 27 publications on potential neuroinvasive or parainfectious neurological complications of COVID-19. The reports focused on smell and taste (n = 5) and evaluation of neurological symptoms and signs in cohorts (n = 5). There were cases of Guillain-Barré syndrome/Miller-Fisher syndrome/cranial neuropathy (seven cases), meningitis/encephalitis (nine cases) and various other conditions (five cases). The number of patients with examination of cerebrospinal fluid and, in particular, SARS-CoV-2 polymerase chain reaction was negligible. Two had a positive SARS-CoV-2 polymerase chain reaction examination of cerebrospinal fluid specimen. Study of potential parenchymal involvement with magnetic resonance imaging was rare. Only four reports received a rating of the highest quality standards. CONCLUSIONS: This systematic review failed to establish comprehensive insights into nervous system manifestations of COVID-19 beyond immune-mediated complications in the aftermath of respiratory symptoms. The authors therefore provide guidance for more careful clinical, diagnostic and epidemiological studies to characterize the manifestations and burden of neurological disease caused by SARS-CoV-2 on behalf of the Infectious Disease Panel of the European Academy of Neurology.