A54-03 Paralysis Unveiled: A Case of Neuromyelitis Optica Spectrum Disorder Responding to Rescue Therapy

Introduction Neuromyelitis optica spectrum disorder (NMOSD) is an autoimmune inflammatory disease thattargets the central nervous system, mainly the optic nerves and spinal cord.¹ It shares certainclinical features with multiple sclerosis, it is now recognized as a separate disorder withdistinctive radiologic characteristics, and clinical outcomes.² The identification of AQP4antibodies and the MRI findings have significantly improved early recognition. Case Presentation A 69-year-old woman with stage IV colorectal cancer and a prior diagnosis of NMOSD (2018)presented with bilateral lower extremity paralysis for the past 24 hours. Vitally signs were stable.Neurological examination revealed 2/5 strength in the lower extremities and decreased sensationfrom T12-L1, with preserved reflexes. Laboratory workup was unremarkable. Serologydemonstrated positive anti-AQP4 antibody (titer 1:100). MRI brain showed scatteredsupratentorial demyelinating plaques (figure. 1) without active lesions. MRI thoracic spinerevealed a large area of hyperintensity extending from T3-T10 (Figure. 2), confirming extensivetransverse myelitis. During hospitalization, the patient’s sensory loss worsened to completeanesthesia below T7 by day 5 of intravenous solumedrol. She was transferred to the ICU forplasmapheresis, completing five sessions with some recovery in neurological deficits. Patientwas discharged home to follow up neurology. Discussion NMOSD is a rare but serious demyelinating disorder, with an estimated incidence ofapproximately one case per 770,000 people annually.¹ Its pathophysiology centers on antibody-mediated astrocyte injury caused by AQP4-IgG, which triggers secondary myelin loss and axonaldamage.² The disease presents with core syndromes such as optic neuritis, longitudinallytransverse myelitis, and brainstem involvement. MRI findings, particularly cord lesions arehighly characteristic and help differentiate NMOSD from multiple sclerosis.¹ Prompt recognitionand management of acute episodes are essential to prevent irreversible neurological injury. High-dose intravenous corticosteroids remain the first-line therapy for acute relapses, while plasmaexchange is used for steroid-refractory or severe cases.² Maintenance therapy with long-termimmunosuppressants such as rituximab effectively reduces relapse frequency and disabilityprogression.¹ Many patients experience incomplete neurological recovery, highlighting thechronic, relapsing nature of the disease. Multidisciplinary follow-up are crucial for optimizingfunctional outcomes and quality of life.² Conclusion NMOSD remains a diagnostic and therapeutic challenge, accurate diagnosis relies on clinical,serologic and imaging features, and a high index of suspicion. Prompt, aggressiveimmunosuppressive therapy is essential to limit irreversible neurological disability Figure 1. Brain MRI: Supratentorialdemyelinating plaques This abstract is funded by: NONE