Anti-MOG antibody associated demyelination masquerading as COVID-19 encephalopathy?

ABSTRACT

Introduction: Acute disseminated encephalomyelitis (ADEM) is a rare autoimmune disease involving inflammation of the brain and spinal cord, usually triggered by a preceding illness or vaccination. We describe a case triggered by SARSCoV-2. Case A previously healthy 1 year old girl presented with reduced GCS, decorticate posturing, seizures and a 3-day history of fever. She required intubation, was started on intravenous antibiotics, Aciclovir and Levetiracetam and was transferred to PICU. PCR nasal swabs revealed the child was SARSCoV-2 and Adenovirus positive. CSF investigations were normal, including a negative SARSCoV-2 RNA. MRI brain showed bilateral widespread T2 and FLAIR signal changes of subcortical white matter and the splenium. Diffusion restriction with T2/FLAIR signal change was noted in the thalami and pons. This was initially felt to be in keeping with Covid-19 encephalopathy, especially given the presence of the splenial lesion. A spinal MR was normal. She made good progress with steroid therapy and at discharge, was able walk a few steps, recognise voices, clap at nursery rhymes, eat and drink normally, but had cortical visual impairment, which is improving. Her anti-MOG antibodies were later found to be positive, which explains the symmetrical scan changes and brainstem involvement. Discussion: In literature, there is a paucity of information regarding COVID-19 related encephalopathy. Lesions in the splenium of the corpus callosum appear to be a relatively consistent finding in children with PIMS-TS. Our child did not have any feature to suggest PIMS-TS. It is likely that SARSCoV-2 triggered off an inflammatory process in this child mediated by MOG antibodies. Conclusion: In the advent of the COVID-19 pandemic, it is important not to attribute clinical findings to SARSCov-2 without excluding other disorders. MOG antibody associated demyelination may mimic the findings described in COVID-19 encephalopathy.