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Chinese Journal of Experimental and Clinical Infectious Diseases(Electronic Edition) ›› 2026, Vol. 20 ›› Issue (02): 122-128. doi: 10.3877/cma.j.issn.1674-1358.2026.02.008

• Case Report • Previous Articles    

A case of myelin oligodendrocyte glycoprotein antibody-associated disease presenting as tumefactive demyelinating lesions

Yifan Cao1, Liangchen Hu2, Ranran Xu2, Chunxia Zhao1, Ziyu Zhang1, Ruolin Li1, Peng Xu2, Xiangyuan Li2,()   

  1. 1 School of Clinical Medicine, Jining Medical University, Jining 272067, China
    2 Department of Neurology, the Affiliated Hospital of Jining Medical University, Jining 272029, China
  • Received:2025-05-15 Online:2026-04-15 Published:2026-06-09
  • Contact: Xiangyuan Li

Abstract:

Objective

To raise the awareness of myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD), which presents as tumefactive demyelinating lesions, and to improve the early diagnosis and treatment, and to avoid the misdiagnosis and inappropriate management.

Methods

The clinical data and management of a patient with MOGAD admitted to the Affiliated Hospital of Jining Medical University on December 30th, 2024 were analyzed, retrospectively, and relevant literature were reviewed.

Results

A 60-year-old female patient presented with dizziness and headache lasting more than 20 days, as well as unsteady gait and aphasia for 6 days, whose clinical presentation was consistent with a brain tumefactive demyelinating lesions. The patient’s serum and cerebrospinal fluid samples were both positive for anti-myelin oligodendrocyte glycoprotein immunoglobulin G (MOG-IgG) antibodies at a titre of 1∶10+. Cranial magnetic resonance imaging (MRI) revealed subcortical brain tissue swelling with abnormal signals in the bilateral temporal and frontal lobes, presenting as tumour-like changes. A diagnosis of MOG-associated demyelinating encephalopathy (MOGAD) was confirmed. The patient was treated with a corticosteroid pulse therapy of 500 mg/d of methylprednisolone, gradually tapered to 62.5 mg/d, followed by combination therapy with the immunosuppressant mycophenolate mofetil capsules, resulting in significant symptom relief. A follow-up MRI performed longer than three months after discharge showed that the abnormal intracranial signals had resolved by approximately 70% compared with the previous scan, with a favourable prognosis.

Conclusions

The clinical presentation of MOG is complex and requires differential diagnosis from other central nervous system disorders, and the importance of MOG-IgG testing must be given high priority to avoid misdiagnosis and inappropriate treatment.

Key words: Tumefactive demyelinating lesions, Myelin oligodendrocyte glycoprotein antibody-associated disease, Clinical manifestation

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