Familiarize providers with the presence of ATM as a neurological sequela of COVID-19 infection. The postulated mechanisms causing ATM associated with SARS-CoV-2 include direct viral neuronal injury and the host’s secondary hyperinflammation syndrome.

To stress the importance of early recognition of underlying COVID-19 infection in patients presenting with ATM for earlier intervention to prevent disease progression.

SARS-CoV-2 enables IL-6 and induces CNS immune responses. Type I IFN is also dysregulated and can affect innate and acquired immunity. In this case series, we present two cases who present with ATM as a complication of COVID-19 infection. First case is a 45yo individual who presented with progressive bilateral lower extremities paresthesia and weakness. Hyperreflexia and motor weakness 4/5 in lower extremities. PMH was significant for recent COVID-19 pneumonia requiring intubation. Additionally, a case of 74yo individual who presented with acute onset of walking difficulty. PMH was significant for recent COVID-19 infection. Hyperreflexia and motor weakness 4/5 in lower extremities with positive Babinski sign. Workup in both cases revealed spinal cord involvement with T2-hyperintense lesions. All workup for other etiologies for ATM like MS, NMO, autoimmune or paraneoplastic syndrome was unremarkable and COVID-19 infection though to be the underlying etiology at this time. Both patients were offered treatment with IV steroids. Decision was made to follow up with serial imaging to start the patient on immunosuppressive therapy if ATM shows any progression.

Those two cases highlights that ATM can present as a sequela to COVID-19 infection or vaccination via the impact SARS-CoV-2 has on the immune system.

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This case series highlights that ATM is not uncommon as a sequela of COVID-19 infection, to familiarize practitioners that probable viral antigen(s) in SARS-CoV-2 target the spinal cord - might present in the COVID-19 vaccine - and may induce immune mechanisms leading to ATM.