Case Presentation: A 36-year-old man with past medical history of recent coronavirus disease 2019 (COVID-19) presented to our hospital with numbness of the lower extremities for two weeks. The patient stated the numbness had progressed from his right leg to his left leg. He also mentioned having urinary and fecal retention. He denied any recent gastroenteritis or stroke but stated he was diagnosed with COVID-19 three months previous where he had shortness of breath, muscle aches, and dry cough. On presentation, his vital signs were normal. A physical exam revealed bilateral 0/5 muscle strength in the lower extremities, decreased sensation to light touch in the lower extremities, and no reflexes of the knees and Achilles. A complete blood count and comprehensive metabolic panel were normal. A serum aquaporin-4 (AQP4) receptor antibody assay was negative. COVID-19 antigen and polymerase chain reaction tests were negative, but a SARS-CoV-2 antibody test was positive. A computed tomography scan of the lumbar spine showed significant urinary bladder distention. A magnetic resonance imaging (MRI) spinal survey showed nonspecific transverse myelitis at the level of thoracic 6 to 8. MRI of the brain showed no acute intracranial abnormality. A lumbar puncture (LP) was performed and was negative for infectious diseases, oligoclonal band, and AQP4 receptor antibodies. The LP also showed normal protein and glucose levels with a slight elevation of neutrophils. The patient was admitted to our hospital for management of acute transverse myelitis (ATM) and neurology was consulted. The patient received five days of intravenous methylprednisolone and seven days of plasmapheresis. The patient was taught how to use an intermittent catheter for his urinary retention. The patient was ultimately stable enough to be discharged home with home health physical therapy, outpatient neurology, and outpatient physical medicine and rehabilitation.

Discussion: Our patient had neurological symptoms and a positive COVID-19 antibody test from a previous infection. This case occurred before the COVID-19 vaccine was available to the general public. We propose that this patient had ATM as a delayed complication of antibodies to SARS-CoV-2. No other cause of ATM could be identified after an extensive work up. The most common neurological symptoms in COVID-19 patients are headache and dizziness (1). However, there have been 43 cases of COVID-19-associated ATM worldwide (2). There is antecedent respiratory, gastrointestinal, or systemic illness in 30% to 60% of idiopathic ATM cases (3). In our case, the patient’s COVID-19 PCR test was negative, but his antibody test was positive. We propose that, like in most post-infection ATM cases, his ATM was likely caused by an overactive immune response and antibody production after COVID-19.

Conclusions: We described a 36-year-old man who developed ATM putatively due to a delayed complication of SARS-CoV-2 antibodies. This case showed that SARS-CoV-2 antibodies could cause complications in other organ systems.

IMAGE 1: MRI of the spinal survey during admission. Heterogeneous enhancement (blue arrow) is seen within the spinal cord extending from the T6-T8 levels without significant associated cord edema extending superiorly and caudally, from the T4-T10 levels.