Myeloradiculitis as an atypical presentation of neuromyelitis optica: a case report

Abstract

Case Presentation: A 39-year-old previously healthy female patient reported paresthesia in the perineal region beginning on April 21, 2025. The symptoms progressed within a few days to paresthesia and severe paresis of the lower limbs, along with urinary retention. She was hospitalized for investigation in May 2025. She denied any history of trauma, vaccination, fever, or systemic symptoms, as well as any suspect family history. Neurological examination revealed predominantly distal and symmetric paresis of the lower limbs with hyperreflexia, reduced proprioception, impaired vibration sense and a sensory level at T10. MRI of the neuraxis showed findings compatible with myeloradiculitis involving the conus medullaris and cauda equina. During investigation, the anti–aquaporin-4 antibody was positive (titer 1:80). After analysis of the cerebrospinal fluid, infectious causes such as schistosomal myeloradiculitis and Elsberg syndrome were excluded, despite the patient’s history of recurrent genital herpes. She was treated with intravenous methylprednisolone 1 g daily for five days, followed by five sessions of plasma exchange on alternate days, and physical therapy. She showed substantial improvement in paresis and partial improvement in sensory ataxia of the lower limbs. Discussion: This is a patient with an atypical presentation of neuromyelitis optica (NMO), an autoimmune disease that affects the central nervous system, mainly resulting in longitudinally extensive myelitis and severe optic neuritis. The diagnosis depends on clinical findings consistent with the disease and ancillary tests, such as MRI of the neuroaxis and orbits, cerebrospinal fluid analysis, and anti-aquaporin-4 antibody testing, which is present in most patients. There are few cases in the literature describing involvement of the nerve roots, which prompted investigation of differential diagnoses. Final Comments: Neuromyelitis optica spectrum disorder (NMOSD) presents a wide range of clinical manifestations and is associated with severe functional outcomes when diagnosis and treatment are delayed. Early and aggressive immunosuppression is essential to minimize the neurological damage.