SARS-CoV-2 infection can trigger myelin oligodendrocyte glycoprotein-related disorders

Coronavirus disease 2019 (COVID-19) causes neurological symptoms. Autoantibodies It can be caused by a host illness.

Background

Myelin oligodendrocyte Glycoprotein-Related Disorders (MOGAD) – The demyelinating state of the central nervous system (CNS) can be monophasic or recurrent and is characterized by the presence of antibodies against myelin oligodendrocyte glycoprotein (MOG).

Due to the high incidence of SARS-CoV-2 immunoglobulin (Ig) G antibody in these patients, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) may induce MOGAD. I have. Another study showed that only 1 in 15 patients after COVID-19 with acute disseminated encephalomyelitis (ADEM) or acute hemorrhagic leukoencephalitis showed anti-MOG positivity.

Recent articles published in Annual clinical and translational neurology report We reported four cases of MOGAD that started after SARS-CoV-2 infection. This paper also highlighted the role of SARS-CoV-2 in the pathogenesis of MOGAD and reviewed previous case reports with similar associations. All four patients were diagnosed with MOGAD post-COVID-19 in Västra Götaland County.

Case 1: Acute disseminated encephalomyelitis

A 25-year-old woman had fever and headache, and SARS-CoV-2 PCR positive was detected. She experienced severe paraplegia, hypoesthesia, loss of consciousness, and two weeks of urinary retention.

Magnetic resonance imaging (MRI) of the brain and spinal cord showed multiple non-enhanced brain parenchyma and spinal cervical-chest high-intensity lesions (T2). Cerebrospinal fluid (CSF) showed two oligoclonal IgG bands.

The patient was diagnosed with ADEM. She started intravenous administration of 1 g of methylprednisolone for 5 days. She had a negative diagnostic test for SARS-CoV-2 and serum IgG aquaporin-4 (AQP4) antibodies, but a positive result for anti-MOG IgG (1: 1000).

MRI was repeated 2 weeks later and showed a new non-contrast enhanced hyperintensity lesion with T2 / fluid decay reversal recovery (FLAIR). These lesions were observed in the progression of intramedullary lesions of the corpus callosum, pons, midbrain, and cervical and thoracic spine, and included contrast enhancement from (thoracic spine) Th6-Th9.

The patient was prescribed a new course of intravenous steroids, followed by a 5-day plasmapheresis session. It was then given a slow taper of methotrexate and oral prednisolone.

After 4 weeks, the patient induced a recurrence of optic neuritis with edema of the optic disc. MRI showed a new lesion in the cerebellar stalk. Patients showed complete radiation (MRI) resolution of brain and spinal cord lesions 4 months after the onset of MOGAD after receiving a new course of high-dose iv steroids.

Patients continue to take prednisolone 10 mg daily and methotrexate 15 mg weekly. She had mild lower limb paresthesia and bladder dysfunction.

Case 2: Bilateral optic neuritis and myelitis

A 20-year-old man was PCR positive for SARS-CoV-2 with mild respiratory symptoms. He had a history of personality disorder and substance abuse. Patients showed a gradual onset of headache, lower back pain, urinary retention, vision loss, photophobia and phonophobia, severe anti-paralysis, and semi-anesthesia 8 weeks after infection.

Neuroophthalmology and OCT showed bilateral optic disc edema, visual impairment, and color vision indicating optic neuritis. The MRI spinal cord showed prominent medulla oblongata T2 lesions from Th9 to the spinal cone, with small localized lesions at Th7 and (cervical) C6 levels, and a slight contrast enhancement at Th9-Th11. The serum MOG antibody test was positive (1: 100 titer), but the anti-AQP4 antibody test was negative.

The patient was negative for infectious or rheumatic findings. He was prescribed plasmapheresis (5 consecutive days) followed by intravenous methylprednisolone 1 g / day for 3 days. Patients then started oral prednisolone tapering to 10 mg / day and 15 mg methotrexate weekly. Six months of treatment led to improvement, and he had only moderate residual paraplegia.

Case 3: Bilateral optic neuritis

A 29-year-old man presented with bilateral visual impairment and frontal headache. He was diagnosed with COVID-19 15 days ago. No other related medical history or medication history was clear.

He was diagnosed with papillitis due to optic neuritis. OCT revealed bilateral optic disc edema. A thorough neurological examination did not induce a deficit. The MRI brain was normal. Lumbar puncture showed normal open pressure, CSF leukocyte, and protein levels, but the oligoclonal IgG band was negative.

Patients started intravenous methylprednisolone 1 g / day for 3 days. The patient was then prescribed oral prednisolone with a tapering dose of 10 mg / day.

Serum AQP4 antibody was negative and anti-MOG IgG was positive (1: 100 titer). One month after treatment, the patient’s eyesight was normal. After 6 weeks of follow-up, the anti-MOG serum titer was 1:10 and was negative 4 months after the diagnosis of optic neuritis.

Case 4: Unilateral optic neuritis

60 year old Chinese woman COVID-19 Symptoms Fever, cold, dyspnea, muscle aches. She was PCR positive for SARS-CoV-2. She was admitted to the intensive care unit (ICU) due to respiratory failure and was supplemented with oxygen. Patients were also given oral betamethasone and rivaloxaban. She was discharged after she improved her symptoms.

54 days after the onset of COVID-19 symptoms, the woman complained of right eye pain and was diagnosed with unilateral optic neuritis with papillitis. On her examination, she had poor eyesight – 20/100.

MRI showed edema and increased contrast in the right optic nerve, but no significant condition in the brain parenchyma or spinal cord. The CSF cell count, albumin, and neurofilament light chain (NfL) were normal and there was no oligoclonal IgG band.

Patients received 1 g / day of methylprednisolone for 3 days, followed by slowly tapering prednisolone. Serological tests revealed negative anti-AQP4 antibodies and positive MOG antibodies (1: 1000 titer).

Conclusion

This paper reports four MOGAD diagnoses immediately after infection with COVID-19. Evidence was consistent with post-infection immune-mediated reactions associated with SARS-CoV-2 infection. The mean latency from the onset of COVID-19 to the onset of MOGAD was 33 days, with a range of 14-56 days. A similar 10-42 day incubation period was observed in patients infected with SARS-CoV-2 who presented with acute transverse myelitis as an immune-mediated reaction after infection.

In conclusion, the development of MOGAD is closely associated with previous COVID-19 and SARS-CoV-2 infections, which has been associated with an increased incidence of MOGAD in Vestra-Yetaland County during a pandemic. rice field.