Coronavirus disease 2019 has led to a global pandemic with the recent demonstration of several neurological manifestations. While there are limited reports of neurologic involvement in the context of COVID-19 infection, recent evidence has established the neuroinvasive potential of the virus.A 57-year-old man was diagnosed with COVID-19 via a polymerase chain reaction test and treated as an outpatient with a combination of prednisone and azithromycin. Nine days after his initial diagnosis, he was admitted to the intensive care unit for acute respiratory failure where he required high-flow oxygen support at a maximum of 60 L/minute. Ten days after his admission to the intensive care unit, he was discharged requiring no oxygen at rest, but 2-3 L/minute with exertion. Nine days after his discharge, he was readmitted with a six-day history of bilateral lower extremity weakness, low back pain, diminished sensation, bowel and bladder incontinence, and decreased rectal sensation and tone. Evaluation for cauda equina syndrome was unremarkable; however, cervical magnetic resonance imaging revealed severe central cervical stenosis of C3-4 and C4-5 with spinal cord flattening and intraparenchymal T2 hyperintensity. The examination was notable for muted reflexes in the bilateral lower extremities, T10 sensory level, decreased rectal tone, and ambulation with a walker. Cerebrospinal fluid analysis revealed an albuminocytologic dissociation. Treatment with intravenous dexamethasone and immunoglobulin resulted in partial motor resolution and complete resolution of his bowel and bladder incontinence within three days of treatment.In the face of this novel global pandemic, surgeons and clinicians should carefully evaluate patients presenting with neurologic deficits and ensure a thorough examination to accurately identify the appropriate etiology for a neurologic deficit.
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