Abstract Introduction Although coronavirus disease 2019 (COVID-19) primarily affects the respiratory system, mounting evidence links SARS-CoV-2 to post-infectious neurologic complications, including acute transverse myelitis (ATM). Proposed mechanisms include immune-mediated demyelination triggered by viral antigen mimicry or cytokine-driven endothelial injury. Early recognition of this rare syndrome is essential because timely corticosteroid therapy can prevent irreversible disability. Case Presentation A 36-year-old Puerto Rican woman with no significant medical history presented with five days of fever, myalgia, and mild cough. SARS-CoV-2 RT-PCR was positive; chest X-ray showed patchy bilateral opacities consistent with mild COVID-19 pneumonia. She was managed supportively and maintained oxygen saturation 94 % on room air. Forty-eight hours later, she developed bilateral upper-extremity weakness, and numbness. On arrival to the emergency department, temperature 38.4 °C, RR 22 breaths/min, HR 109 bpm, and SpO2 95 % RA. Neurologic examination revealed paraparesis (3/5), hyperreflexia, and decreased sensation in upper extremities; cranial nerves were normal. Laboratory results showed leukocytosis (14.2 K/µL) and elevated inflammatory markers; metabolic, infectious (HIV, syphilis, B12, folate), and autoimmune panels were unremarkable. Lumbar puncture revealed mild lymphocytic pleocytosis and elevated protein (81 mg/dL) with normal glucose; CSF multiplex PCR was negative for neurotropic pathogens. Cervicothoracic spine MRI demonstrated a longitudinally extensive T2-hyperintense lesion from C2 to C5 without cord compression, or hemorrhage, or neoplasm; brain MRI was normal. Diagnosis of post-COVID-19 transverse myelitis was made and the patient received intravenous methylprednisolone 1 g daily × 5 days followed by an oral taper, with rapid neurologic improvement. At six-week follow-up, bilateral upper-extremity strength improved to 4+/5 and sensory deficits markedly decreased.DiscussionSARS-CoV-2-related ATM is thought to represent a post-infectious immune response rather than direct viral invasion, supported by negative CSF PCR and delayed neurologic onset after respiratory illness. Reported imaging typically reveals spinal longitudinally extensive lesions ≥ 3 vertebral segments, paralleling our findings. Early administration of high-dose corticosteroids remains first-line therapy; plasma exchange or IVIG is reserved for incomplete recovery. This case underscores that clinicians managing COVID-19 should maintain vigilance for abrupt motor or sensory deficits, even in patients with mild pulmonary involvement. Integration of pulmonary, neurologic, and radiologic data is vital for timely diagnosis and rehabilitation planning. Conclusion COVID-19 can trigger post-infectious transverse myelitis, linking pulmonary infection to spinal cord inflammation. Prompt recognition, spinal MRI, and immunosuppressive therapy are crucial for favorable outcomes. Multidisciplinary coordination between pulmonology, neurology, and rehabilitation teams can reduce long-term disability following SARS-CoV-2 infection. This abstract is funded by: None
Gines et al. (Fri,) studied this question.