ABSTRACT
A 23-year-old man presented with headache, fever, and urinary retention. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) antigen tests were positive, but SARS-CoV-2 polymerase chain reaction (PCR) results were negative. MRI showed long spinal cord lesions. Due to positive serum and cerebrospinal fluid myelin oligodendrocyte glycoprotein (MOG) antibodies, we made the diagnosis of MOG-associated disease. We concluded that the antigen tests were false positives because SARS-CoV-2 IgM and IgG were not elevated. Although the mechanism behind the false-positive results is unclear, physicians should consider the possibility of a false-positive result in the SARS-CoV-2 antigen test.
ABSTRACT
Myelin oligodendrocyte glycoprotein (MOG) antibody has been associated with a wide range of neurological diseases, from neuromyelitis optica spectrum disorder to acute disseminated encephalomyelitis. However, MOG positivity with isolated encephalitis has been infrequently reported. MRI findings are usually of the demyelination type. In this case, we report on a patient with COVID-19 exposure who presented with altered mental status and multiple ring-enhancing lesions on MRI mimicking metastatic disease. Due to his unusual MRI findings and presentation, the correct diagnosis was not apparent until MOG antibody results came back positive.
ABSTRACT
The coronavirus disease 2019 (COVID-19) includes an extensive spectrum of clinical manifestations of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Previous studies have shown that SARS-CoV-2 often exhibits central nervous system (CNS) manifestations, including encephalitis, meningitis, and spinal cord pathologies. To date, few cases of COVID-19-associated transverse myelitis (TM) have been described. A 40-year-old unvaccinated man with no significant medical history presented to the emergency department complaining of fever, worsening burning sensation in his lower extremities, unsteady gait, and difficulty initiating urination for five days. Twelve days before presentation, the patient had tested positive for SARS-CoV-2 infection. Physical examination revealed hyperesthesia, starting around the nipple line (T4) and extending distally, involving the lower extremities, accompanied by symmetric weakness in the lower extremities. Magnetic resonance imaging of the thoracic spine with and without contrast revealed mild intramedullary signal abnormality at T3-T4 and T6-T8, confirming the suspicion of TM. Further laboratory testing revealed a C-reactive protein level of 67 mg/L, lactate dehydrogenase level of 181 mg/L, serum B12 level of 781 pg/mL, methylmalonic acid level of 165 nmol/L, folate of >24.5 ng/mL, and thyroid-stimulating hormone level of 0.481 µIU/L. Lumbar puncture was performed, and cerebrospinal fluid analysis revealed a cell count of 14 cells/µL, with 69% lymphocytes, glucose level of 81 mg/dL, protein level of 32 mg/dL, and negative cultures. Human immunodeficiency virus, antinuclear antibody screening, anti-DNA, rapid plasma reagin, Lyme serology, anti-SSA, and anti-SSB antibodies were unremarkable. Serum aquaporin-4 immunoglobulin G was negative, and myelin oligodendrocyte glycoprotein (MOG) antibodies were positive. The patient was treated with intravenous methylprednisolone and oral gabapentin and was discharged after five days when his urinary retention improved. Most previously reported cases of COVID-19-related TM were negative for autoimmune workup. Although the exact pathophysiology of COVID-19-related TM remains unclear, one hypothesis suggests that it is a consequence of the direct viral invasion. However, our patient had MOG antibodies, suggesting the possible involvement of a different mechanism. In MOG-associated TM, it has been suggested that MOG antibodies gain access to the CNS through disruption of the blood-brain barrier. This unique presentation demonstrates that further studies are needed to understand the effects of SARS-CoV-2 infection on the immune and nervous systems. It also highlights that young and otherwise healthy patients are at risk of severe COVID-19-related complications, including CNS disorders.
ABSTRACT
Myelin oligodendrocyte glycoprotein (MOG) antibody-associated disorder (MOGAD) is a newly identified autoimmune demyelinating disorder that is often associated with acute disseminated encephalomyelitis and usually occurs postinfection or postvaccination. Here we report a case of MOGAD after mRNA severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) vaccination. A previously healthy 68-year-old woman presented to our department with gradually worsening numbness on the right side of her face, which began 14 days after her second dose of an mRNA-1273 vaccination. The patient's brain MRI revealed a right cerebellar peduncle lesion with gadolinium enhancement, a typical finding of MOGAD. A neurological examination revealed paresthesia on her right V2 and V3 areas. Other neurological examinations were unremarkable. Laboratory workups were positive for serum MOG-IgG as assessed by live cell-based assays and the presence of oligoclonal bands in the cerebrospinal fluid (CSF). The patient's serum test results for cytoplasmic-antineutrophil cytoplasmic antibodies, perinuclear-cytoplasmic-antineutrophil cytoplasmic antibodies, GQ1b-antibodies, and aquaporin-4 antibodies (AQP4-IgG) were all negative. Tests for soluble interleukin (IL)-2 receptors in the serum, IL-6 in the CSF and skin pricks, and angiotensin converting enzyme tests were all unremarkable. The patient was diagnosed with MOGAD after receiving an mRNA SARS-CoV-2 vaccination. After two courses of intravenous methylprednisolone treatment, the patient's symptoms improved and her cerebellar peduncle lesion shrunk slightly without gadolinium enhancement. To date, there have only been two cases of monophasic MOGAD following SARS-CoV-2 vaccination, including both the ChAdOx1 nCOV-19 and mRNA-1273 vaccines, and the prognosis is generally similar to other typical MOGAD cases. Although the appearance of MOG antibodies is relatively rare in post-COVID-19-vaccine demyelinating diseases, MOGAD should be considered in patients with central nervous system (CNS) demyelinating diseases after receiving a SARS-CoV-2 vaccine.
ABSTRACT
Severe acute respiratory syndrome coronavirus-2 (SARS-Cov-2) may cause various neuro-ophthalmologic manifestations including optic perineuritis. Optic perineuritis is a rare form of orbital inflammatory disease in which optic nerve sheath is inflamed and nonspecific fibrotic thickening with classic radiological finding is a perineural enhancement of optic nerve sheath. A 45-year-old gentleman with known diabetes mellitus, hypertension and dyslipidemia was admitted with a critically ill COVID-19 infection. During the recovery period, the patient developed sudden onset of painless loss of vision. MRI head and orbit with gadolinium was suggestive of optic perineuritis. Other secondary causes of autoimmune or vasculitis myelin oligodendrocyte glycoprotein (MOG) antibody disease and other common central nervous system (CNS) infection were excluded. The patient had dramatic response with steroids. This is the first rare case report of COVID-19-related optic perineuritis in critically ill COVID-19 patients with seronegative MOG antibody. Optic perineuritis is a rare orbital inflammatory disease and underlying mechanisms may arise from systemic response to COVID-19 infection as well as direct effects of the virus via angiotensin-converting enzyme 2 (ACE-2) receptors on ocular tissues. Optic perineuritis is a rare disease with inflammation restricted to the optic nerve sheath. Neuroimaging of the brain and orbit is the most important modality of choice for visualizing optic nerve sheath and optic nerve. Delay in the diagnosis of COVID-19-related optic perineuritis, may result in permanent optic nerve injury and irreversible vision loss.
ABSTRACT
Neurological manifestations of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) are relatively common. Although some may be consequences of direct cellular viral invasion (neurotropism), many represent post-infectious inflammation mediated by autoimmune mechanisms. We herein report the case of a 69-year-old diabetic male who presented with bilateral sub-acute, progressive loss of vision 45 days after suffering a presumed SARS-CoV-2 related pneumonia. He had bilateral optic disc oedema. Magnetic resonance imaging showed uniform contrast enhancement of both optic nerves without spinal cord involvement. He tested positive for SARS-CoV-2 IgG and myelin oligodendrocyte glycoprotein (MOG) IgG antibodies. He was treated with intravenous methylprednisolone for 5 days. The optic disc oedema resolved within 6 weeks with improvement in visual acuity, although optic atrophy developed by week 16. The MOG-IgG antibody test turned negative after 24 weeks.
ABSTRACT
A 39-year-old lady with relapsing myelin oligodendrocyte glycoprotein antibody (MOG-IgG) associated disease developed coryzal symptoms, malaise, sweating, and postural dizziness. Six days later she presented with painful progressive right visual loss consistent with optic neuritis. COVID-19 was confirmed by nasopharyngeal swab and MOG-IgG serological reversion was noted. Visual function improved following steroids and plasma exchange. This case highlights a possible causal association between inflammation due to COVID-19 and a relapse of MOG-IgG associated disease. It also highlights the clinical relevance of reporting MOG-IgG titers in MOG-IgG associated disease.