Seasonal distribution of relapses in MOG antibody associated disease (MOGAD)

Introduction: The influence of environmental factors on central nervous system demyelinating conditions have been recently studied. In MOG antibody associated disease (MOGAD), a seasonal distribution of relapses is not yet well-defined. Objective(s):: To investigate the presence of seasonal distribution of MOGAD relapses. Method(s): Prospective data from consented MOGAD patients within the Oxford National NMO Highly Specialised Service were analysed until April 2022. Demographic and clinical characteristics, including relapse date and phenotype, were recorded. All relapses with month-defined dates were used to calculate observed monthly frequencies. Expected frequencies were calculated assuming an uniform distribution throughout the year, adjusting for month's length and patient numbers under follow up. Any deviation from a uniform distribution was analysed, and seasonal peaks were assessed using Friedman's, Edward's, Ratchet circular scan and Hewitt's rank-sum tests. Result(s): Three-hundred-four MOGAD patients were included, 190 (62.5%) females, mean age at onset 31 years (SD 16.9), median disease duration 3.0 (IQR 5.0) years, 77 (25.3%) with paediatric age onset. No significant seasonal pattern was identified when analysing all relapses (n=691), or onset relapses (n=286). Regarding age of disease onset, no seasonal pattern was found in onset under 18 (n=483) or over 18 years old (n=208). Regarding phenotype, no seasonal pattern was found in optic neuritis (n=483), transverse myelitis (n=180) or brain and brainstem relapses (n=125). Analysing all the relapses from the start of the COVID-19 pandemic (March 2020 - February 2022, n=112), a seasonal peak was identified from March to May (V(N)=0.132, p<0.05). Conclusion(s): No seasonal pattern of relapses in MOGAD was noted until the COVID-19 pandemic started in the UK. Seasonal infection peaks during winter and subsequent lockdowns could have influenced MOGAD relapse rates in the past two years.

Acute demyelinating events triggered by COVID-19 vaccines: Case series

Introduction: The United Kingdom (UK) was one of the first countries in the world providing mRNA (Pfizer-BioNTech) and adenovirus-based (Oxford-AstraZeneca) vaccines against SARSCoV- 2 for its population. By mid-May 2021, over 36 million British citizens had received at least one dose of COVID-19 vaccine. Aim: We described clinical, MRI, laboratory features, therapy, and outcomes of five COVID-19 vaccine-related cases of acute demyelinating events with onset between February and May 2021. Case 1: A 57-year-old man presented paraparesis, instability and bladder dysfunction 2 weeks after AstraZeneca vaccine jab. MRI showed lesions in the brainstem, cerebellum and cerebral hemispheres and a C3-C6 lesion. Myelin-oligodendrocyte-glycoprotein IgG (MOG-IgG) were positive. Incomplete recovery after 1 month. Case 2: A 36-year-old lady developed traverse myelitis (TM) and left optic neuritis (ON) after 2 weeks from Pfizer vaccine jab. MRI showed enhancement of left optic nerve and T10-T11 and T12-conus lesions. Oligoclonal bands (OCBs) restricted in cerebrospinal fluid (CSF) were found. MOG-IgG, aquaporin-4-IgG (AQP4-IgG) were negative. Incomplete recovery after 1 month . Case 3: A 50-year-old lady presented bilateral facial weakness and visual loss after 10 days from AstraZeneca vaccine jab. Visual acuity was reduced in both eyes. MRI showed enhancement along the facial nerves. MOG-IgG, AQP4-IgG and OCBs were negative. Incomplete recovery after 1 month. Case 4: A 44-year-old man, 2 weeks following AstraZeneca vaccine, developed progressive dyspnoea, chest pain and diplopia with rapid deterioration to quadriplegia and respiratory failure requiring mechanical ventilation. MRI showed bilateral multiple lesions involving cerebral hemispheres, thalami, brainstem and spinal cord. MOG-IgG, AQP-4 IgG and OCBs were negative. The patient died. Case 5: A 57-year-old lady with seronegative relapsing TM since 2009 and fulfilling neither multiple sclerosis nor NMOSD diagnostic criteria. After 1 week from AstraZeneca vaccine jab, she presented TM symptoms and a new active T9-T10 lesion. Poor recovery after 2 months. Conclusions: It is currently unclear whether the association is greater than chance or whether the Oxford-AstraZeneca vaccine has a greater incidence because used more frequently in the UK than the Pfizer vaccine. However, viral illnesses and vaccinations have been reported to trigger demyelinating events, including MOG-IgG disease, associated with ADEM.