Acute Flaccid Myelitis in a Pediatric Patient With Coronavirus Disease 2019.

The etiology of acute flaccid myelitis (AFM) has yet to be determined. Viral link has been suggested, but severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)-associated AFM has not been reported in children. We describe a three-year-old boy, with AFM associated with coronavirus disease 2019 (COVID-19) infection. In the era of COVID-19 pandemic, patients with AFM should be tested for SARS-CoV-2.

Anti-myelin Oligodendrocyte Glycoprotein Antibody-positive Myelitis after Coronavirus Disease 2019.

We herein report a case of anti-myelin oligodendrocyte glycoprotein (MOG) antibody-related myelitis caused by coronavirus disease (COVID-19) infection in 2021. A 22-year-old man with no history of any related illness contracted COVID-19. Eight days later, he developed bladder problems, paraplegia and sensory disturbances. Cervical spinal cord magnetic resonance imaging revealed extensive hyperintensity at T2 and spinal cord lesions extending from C4 to Th1. The patient was diagnosed with transverse myelitis and started on intravenous methylprednisolone, plasma exchange and intravenous immunoglobulin therapy. The symptoms improved only after intravenous methylprednisolone therapy. Anti-MOG antibodies were found in his serum and cerebrospinal fluid during routine screening. As this observation is unusual and could cause serious health problems, we wonder if COVID-19 triggered this autoimmune response.

A disproportionality analysis for the association of central nervous system demyelinating diseases with COVID-19 vaccination using the World Health Organization pharmacovigilance database.

BACKGROUND: Limited information is available on associations between COVID-19 vaccines and central nervous system (CNS) demyelinating diseases. OBJECTIVES: We investigated potential safety signals for CNS demyelinating diseases related to COVID-19 vaccines using the World Health Organization pharmacovigilance database. METHODS: Disproportionality analyses of CNS demyelinating disease following COVID-19 vaccination were performed by calculating the information component (IC) or the reporting odds ratio (ROR) compared with those for the entire database and for all other viral vaccines. RESULTS: We identified 715 cases of optic neuritis, 515 of myelitis, 220 of acute disseminated encephalomyelitis (ADEM), and 2840 total CNS demyelinating events adverse drug reactions from July 2020 through February 2022. For mRNA-based and ChAdOx1 nCoV-19 vaccines, there were no potential safety signals of disproportionality for optic neuritis (IC₀₂₅ = -0.93, ROR₀₂₅ = 0.38; IC₀₂₅ = -1.76, ROR₀₂₅ = 0.26), myelitis (IC₀₂₅ = -0.69, ROR₀₂₅ = 0.50; IC₀₂₅ = -0.63, ROR₀₂₅ = 0.53), ADEM (IC₀₂₅ = -1.05, ROR₀₂₅ = 0.33; IC₀₂₅ = -1.76, ROR₀₂₅ = 0.20), or overall CNS demyelinating disease events (IC₀₂₅ = -0.66, ROR₀₂₅ = 0.52; IC₀₂₅ = -1.31, ROR₀₂₅ = 0.34) compared with other viral vaccines. CONCLUSION: As with other viral vaccines, our disproportionality analyses indicate that the risk of COVID-19 vaccine-associated CNS demyelinating disease was low.

A Case of Elsberg Syndrome in the Setting of Asymptomatic SARS-CoV-2 Infection.

ABSTRACT: Elsberg syndrome is a rare cause of lumbosacral radiculitis with concomitant thoracic and lumbosacral myelitis that can be seen after an acute or reactivated viral infection. After the initial coronavirus surge in New York City, a 68-year-old man developed progressive lower extremity weakness and a defined sensory level at the lower abdomen. He had highly elevated SARS-CoV-2 IgG antibodies despite an absence of preceding COVID-19 symptoms. Serial electrodiagnostic testing revealed absent lower extremity late responses, with otherwise normal distal sensorimotor conductions. Electromyography revealed active neurogenic changes and reduced motor unit recruitment in the L3-L4 myotomes. Treatment with methylprednisolone and intravenous immunoglobulin was followed by minimal clinical improvement but re-emergence of the lower extremity late responses on electrodiagnostic testing. We report here, to the best of our knowledge, the first case of suspected COVID-19-associated Elsberg syndrome, which expands the spectrum of neuromuscular manifestations associated with SARS-CoV-2 infection and sheds light on ways to approach diagnostic and treatment options for these patients.

Neurological manifestations associated with SARS-CoV-2 and other coronaviruses: A narrative review for clinicians.

INTRODUCTION: The past two decades have been marked by three epidemics linked to emerging coronaviruses. The COVID-19 pandemic highlighted the existence of neurological manifestations associated with SARS-CoV-2 infection and raised the question of the neuropathogenicity of coronaviruses. The aim of this review was to summarize the current data about neurological manifestations and diseases linked to human coronaviruses. MATERIAL AND METHODS: Articles have been identified by searches of PubMed and Google scholar up to September 25, 2020, using a combination of coronavirus and neurology search terms and adding relevant references in the articles. RESULTS: We found five cohorts providing prevalence data of neurological symptoms among a total of 2533 hospitalized COVID-19 patients, and articles focusing on COVID-19 patients with neurological manifestations including a total of 580 patients. Neurological symptoms involved up to 73% of COVID-19 hospitalized patients, and were mostly headache, myalgias and impaired consciousness. Central nervous system (CNS) manifestations reported in COVID-19 were mostly non-specific encephalopathies that represented between 13% and 40% of all neurological manifestations; post-infectious syndromes including acute demyelinating encephalomyelitis (ADEM, n=13), acute necrotizing encephalopathy (ANE, n=4), Bickerstaff's encephalitis (n=5), generalized myoclonus (n=3) and acute transverse myelitis (n=7); other encephalitis including limbic encephalitis (n=9) and miscellaneous encephalitis with variable radiologic findings (n=26); acute cerebrovascular diseases including ischemic strokes (between 1.3% and 4.7% of COVID-19 patients), hemorrhagic strokes (n=17), cerebral venous thrombosis (n=8) and posterior reversible encephalopathy (n=5). Peripheral nervous system (PNS) manifestations reported in COVID-19 were the following: Guillain-Barré syndrome (n=31) and variants including Miller Fisher syndrome (n=3), polyneuritis cranialis (n=2) and facial diplegia (n=2); isolated oculomotor neuropathy (n=6); critical illness myopathy (n=6). Neuropathological studies in COVID-19 patients demonstrated different patterns of CNS damage, mostly ischemic and hemorrhagic changes with few cases of inflammatory injuries. Only one case suggested SARS-CoV-2 infiltration in endothelial and neural cells. We found 10 case reports or case series describing 22 patients with neurological manifestations associated with other human coronaviruses. Among them we found four MERS patients with ADEM or Bickerstaff's encephalitis, two SARS patients with encephalitis who had a positive SARS-CoV PCR in cerebrospinal fluid, five patients with ischemic strokes associated with SARS, eight MERS patients with critical illness neuromyopathy and one MERS patient with Guillain-Barré Syndrome. An autopsy study on SARS-CoV patients demonstrated the presence of the virus in the brain of eight patients. CONCLUSION: The wide range of neurological manifestations and diseases associated with SARS-CoV-2 is consistent with multiple pathogenic pathways including post-infectious mechanisms, septic-associated encephalopathies, coagulopathy or endothelitis. There was no definite evidence to support direct neuropathogenicity of SARS-CoV-2.