Seronegative Myelitis with Overlapping NMOSD, MOGAD, And Multiple Sclerosis Features: A Case Report

Case Report

Seronegative Myelitis with Overlapping NMOSD, MOGAD, And Multiple Sclerosis Features: A Case Report

  • Zaid Mateen
  • Rachel Yim
  • Leonard B. Goldstein ID *

A.T. Still University, School of Osteopathic Medicine in Arizona, Mesa, United States America.

*Corresponding Author: Leonard B. Goldstein, A.T. Still University, School of Osteopathic Medicine in Arizona, Mesa, United States America.

Citation: Mateen Z, Yim R, Goldstein LB. (2026). Seronegative Myelitis with Overlapping NMOSD, MOGAD, And Multiple Sclerosis Features: A Case Report, International Clinical and Medical Case Reports, BioRes Scientia Publishers. 5(2):1-4. DOI: 10.59657/2837-5998.brs.26.065

Copyright: © 2026 Leonard B. Goldstein, this is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Received: June 01, 2026 | Accepted: June 29, 2026 | Published: July 07, 2026

Abstract

A 43-year-old man with recurrent longitudinally extensive transverse myelitis (LETM) who presented with progressive lower-extremity weakness, urinary incontinence, and falls following an initial steroid-responsive episode. Repeat magnetic resonance imaging demonstrated new enhancing cervical cord lesions and multifocal cerebral lesions despite negative aquaporin-4 and myelin oligodendrocyte glycoprotein antibody testing. Treatment with high-dose intravenous corticosteroids and plasma exchange resulted in significant neurologic improvement, followed by inpatient rehabilitation. This case highlights the diagnostic challenges of recurrent LETM and underscores the importance of timely immunotherapy escalation and early rehabilitation in promoting functional recovery despite diagnostic uncertainty.


Keywords: longitudinally extensive transverse myelitis; neuromyelitis optica spectrum disorder; myelin oligodendrocyte glycoprotein antibody disease; plasma exchange; demyelinating disease

Introduction

Inflammatory myelopathies require early etiologic stratification because diagnosis influences acute treatment decisions, relapse prevention strategies, prognosis, and rehabilitation planning [1-3]. Longitudinally extensive transverse myelitis (LETM), typically defined as a spinal cord lesion extending three or more vertebral segments, is most commonly associated with NMOSD and is also reported in MOGAD, ADEM, sarcoidosis, and infectious myelitis, while being less typical of conventional multiple sclerosis [1-5]. Interval clinical or radiographic progression following an initial episode should prompt reassessment of the underlying disease process [1-5].

We report a case of recurrent LETM with new enhancing cervical spinal cord lesions and evolving multifocal cerebral lesions treated with high-dose corticosteroids, plasma exchange, and subsequent inpatient rehabilitation, highlighting functional recovery despite persistent diagnostic uncertainty.

Case Presentation

Clinical History

A 43-year-old man with obstructive sleep apnea and a prior diagnosis of transverse myelitis (November 2025) presented with two weeks of progressive bilateral lower-extremity weakness and urinary incontinence with intermittent cramping. He reported mechanical falls due to his legs “giving out,” difficulty rising from a squat, and concern about driving due to delayed braking.

During the initial episode, he presented with bilateral leg weakness, erectile dysfunction, and decreased rectal tone. Thoracic spine MRI demonstrated a longitudinally extensive lesion spanning T2-T7, and brain MRI demonstrated a left temporal T2/FLAIR hyperintensity. Lumbar puncture reportedly showed absence of oligoclonal bands. Serum MOG-IgG and AQP4-IgG testing was documented as negative. He partially improved following a five-day course of intravenous methylprednisolone and was discharged on an oral prednisone taper.

Approximately two weeks after completing the taper, he developed recurrent and progressive neurologic deficits prompting re-presentation.

Examination

Neurologic examinations documented diffuse hyperreflexia, bilateral Hoffmann signs, fluctuating lower-extremity weakness, and a sensory level initially around T5 with subsequent rostral fluctuation. Upper-extremity strength was initially preserved, with later reports of right-hand clumsiness and mild grip weakness. Cranial nerve testing was unremarkable.

Diagnostic Studies

MRI performed January 13, 2026 demonstrated new enhancing cervical spinal cord lesions at C4 and C7 and new multifocal supratentorial T2/FLAIR lesions compared with prior imaging. The radiologic differential included NMOSD, MS, ADEM, sarcoidosis, and other autoimmune demyelinating disorders [1-5,8].

Hospital Course and Treatment

Given severe neurologic deficits with interval radiographic progression, the patient received intravenous methylprednisolone (1 g daily for five days). Plasma exchange was initiated with five sessions planned every other day. During hospitalization, neurologic deficits fluctuated, with a documented near-complete loss of lower-extremity movement and a high sensory level. Following completion of corticosteroids and plasma exchange, he demonstrated progressive improvement in lower-extremity strength and bowel and bladder control.

He was transitioned to oral prednisone with a taper plan and discharged to acute inpatient rehabilitation while beginning to stand with approximately 3/5-4/5 lower-extremity strength.

Discussion

Diagnostic Considerations in Recurrent LETM

Recurrent LETM with new cervical cord enhancement and evolving multifocal brain lesions supported an inflammatory demyelinating disorder extending beyond an isolated spinal relapse. LETM is a characteristic imaging feature of NMOSD and is also well described in MOGAD, while being less typical of conventional MS [1-5,8].

MOGAD was considered given LETM, multifocal CNS involvement, and substantial functional improvement following immunotherapy, although repeat negative serum MOG-IgG testing reduced diagnostic confidence [3,9]. NMOSD was also considered, as recurrent severe myelitis with longitudinal involvement is characteristic of the disorder; the absence of optic neuritis and negative AQP4-IgG testing lowered probability without excluding AQP4-IgG-negative NMOSD [1,2]. MS was considered less typical given early LETM, severity of deficits, and absence of cerebrospinal fluid oligoclonal bands, though aggressive MS variants remained part of the differential [6,7,10]. ADEM was considered less likely based on the adult presentation, lack of encephalopathy, and recurrent course [5,11].

Alternative Diagnoses

Cauda equina syndrome was considered but was inconsistent with upper motor neuron signs and intramedullary spinal cord lesions rather than lumbosacral nerve root compression [16,17,21,22]. Guillain-Barré syndrome was also considered but was inconsistent with preserved reflexes, a defined sensory level, and central nervous system imaging abnormalities [18-20].

Rationale for Escalation and Rehabilitation Relevance

High-dose intravenous corticosteroids are commonly used as first-line therapy for severe acute demyelinating attacks [1-3]. In cases of significant or progressive neurologic deficits, plasma exchange is supported as rescue therapy by neurologic and therapeutic guidelines [12-14].

Severe inflammatory myelitis is associated with abrupt functional decline, secondary complications, and prolonged disability risk [15]. Early physiatric involvement and coordinated inpatient rehabilitation are associated with improved functional outcomes, prevention of complications, and safe discharge planning in patients with severe spinal cord and demyelinating disorders [15]. This case demonstrates that meaningful functional recovery can occur despite diagnostic uncertainty when rehabilitation planning is integrated early in the disease course.

Conclusion

Recurrent LETM with radiographic progression should prompt reassessment for inflammatory demyelinating disorders even when antibody testing is negative. In severe presentations, escalation from corticosteroids to plasma exchange may be appropriate. Diagnostic uncertainty does not preclude meaningful functional recovery, and early integration of physiatric care and inpatient rehabilitation can support neurologic and functional improvement.

Highlights

  • Recurrent longitudinally extensive myelitis with new enhancing cervical cord lesions prompted reassessment beyond an isolated spinal relapse.
  • Negative MOG-IgG and AQP4-IgG testing limited diagnostic certainty despite clinical and radiographic features overlapping with NMOSD and MOGAD.
  • Escalation from high-dose corticosteroids to plasma exchange was consistent with rescue therapy used for severe inflammatory demyelinating attacks.
  • Functional recovery progressed from near-paralysis to supported standing with partial lower-extremity strength and improving bowel and bladder control, supporting early physiatric involvement and inpatient rehabilitation placement.

Statement of Informed Consent

Informed consent was obtained from the patient that was presented in the case report.

References