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Seronegative Longitudinally Extensive Transverse Myelitis in a Filipino Adult: Diagnostic Challenges and
Mary Grace S Aguda-Barillo1, Jon Stewart H Dy1,2,3, Jasmyn A De Leon4,5,1
1Neurology, Chinese General Hospital and Medical Center, Manila, PHL.
None:
Longitudinally extensive transverse myelitis (LETM) is a radiologic pattern of longitudinal spinal cord involvement most commonly associated with antibody-mediated autoimmune diseases such as neuromyelitis optica spectrum disorder and myelin oligodendrocyte glycoprotein antibody-associated disease. Seronegative inflammatory cases remain diagnostically challenging because they require careful exclusion of infectious, autoimmune, vascular, neoplastic, metabolic, and structural etiologies. A 45-year-old Filipino female presented with a three-day history of severe upper back pain, followed by rapidly progressive bilateral upper and lower extremity weakness, sensory disturbances, and urinary retention. Neurologic examination revealed asymmetric quadriparesis, a sensory level at the fourth thoracic dermatome, preserved vibration and proprioception, and mixed hyperreflexia and hyporeflexia with bilateral Babinski signs. Spinal magnetic resonance imaging (MRI) demonstrated a poorly defined, non-expansile intramedullary T2-hyperintense lesion extending contiguously from C3 to T2 without discrete enhancement. Diffusion-weighted imaging demonstrated no restricted diffusion. Cerebrospinal fluid analysis showed mild lymphocytic pleocytosis with normal IgG index and absence of oligoclonal bands. Extensive infectious, inflammatory, autoimmune, and metabolic investigations were unrevealing, including negative serum aquaporin-4 and myelin oligodendrocyte glycoprotein antibodies. Follow-up spinal MRI performed 3.5 months later demonstrated persistent longitudinal non-enhancing intramedullary T2 hyperintensity with evolution toward chronic myelomalacic change, providing important longitudinal imaging evidence supporting an inflammatory antibody-negative myelopathy over competing diagnostic considerations. The patient was treated with high-dose intravenous methylprednisolone, followed by an oral prednisone taper and subsequent initiation of azathioprine because of persistent severe deficits. Despite immunotherapy and rehabilitation, she remained wheelchair-dependent with persistent dysesthesias and neurogenic bladder at follow-up. Following comprehensive multidisciplinary evaluation and longitudinal follow-up, an inflammatory antibody-negative LETM was considered the most likely diagnosis after exclusion of competing etiologies. This case highlights the diagnostic complexity, therapeutic challenges, and potentially severe neurologic outcomes associated with seronegative LETM. It also underscores the importance of systematic exclusion of alternative etiologies, longitudinal follow-up, repeat serologic evaluation, and individualized consideration of escalation immunotherapy in patients with incomplete response to corticosteroid treatment.

