6th Edition of Neurology World Conference 2026

Speakers - NWC 2026

Madison S Meyer, Neurology World Conference,Miami,USA

Madison S Meyer

Madison S Meyer

  • Designation: Wayne State University School of Medicine Department of Medicine Detroit
  • Country: USA
  • Title: Neuromyelitis Optica Presenting With Mammillary Body and Cervicomedullary Lesions After Severe Hyponatremia Mimicking Osmotic Demyelination Syndrome

Abstract

Neuromyelitis optica spectrum disorder (NMOSD) is an autoimmune disease characterized by demyelination, most commonly of the optic nerves and spinal cord but can affect other central nervous system structures. Some variants of NMOSD have overlapping radiographic features with metabolic and osmotic demyelination processes. We present a case of NMOSD with unusual radiographic findings involving the bilateral mammillary bodies and cervicomedullary dorsal columns that mimicked osmotic demyelination syndrome. A 54-year-old woman with a history of hypertension and Roux-en-Y gastric bypass developed acute numbness, weakness, dizziness, and blurred vision associated with hyponatremia. She was admitted for observation during correction of symptomatic hypoosmolar hyponatremia. Brain MRI showed high fluid-attenuated inversion recovery (FLAIR) signal within bilateral mammillary bodies and dorsomedial columns of the upper cervical cord without diffusion restriction. She was discharged after improvement with resolution of hyponatremia and symptomatic improvement. A few weeks later she was readmitted with complaints of right-sided facial pain and numbness, as well as intermittent stabbing dysesthesias in both lower extremities. MRI brain and cervical spine showed progression of FLAIR hyperintensity to involve the bilateral mammillary bodies, cervicomedullary dorsal columns, and now with patchy enhancement involving the cervicomedullary junction as well as a new hyperintense dorsal column signal abnormality at the level of C2–C3 without diffusion restriction. Cerebrospinal fluid studies were unrevealing. Given the recent history of severe hyponatremia and involvement of metabolically vulnerable structures, osmotic demyelination syndrome was considered but was less likely given interval progression of lesions as well as presence of contrast enhancement. Serum testing revealed antibodies against aquaporin-4. The patient was diagnosed with NMOSD and treated with intravenous methylprednisolone followed by intravenous immunoglobulin therapy with improvement of symptoms and resolution of dysesthesias with improvement in ambulation. NMOSD can present with rare radiographic variants that can closely mimic osmotic demyelination syndrome as demonstrated in our case. It is crucial that clinicians be able to distinguish between the two entities as autoimmune demyelinating diseases require immunomodulatory treatment while osmotic demyelination syndrome primarily requires supportive management. If lesions are involving metabolically susceptible structures on brain MRI but enhancement or interval progression is identified, NMOSD should be considered