MOG antibody associated disease (MOGAD) presenting with extensive brain stem encephalitis: A case report

Olbert, Elisabeth; Brunner, Cornelia; Alhani, Naela; Našel, Christian; Struhal, Walter

doi:10.1016/j.ensci.2022.100432

Cited by 2 publications

(2 citation statements)

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“…[7] A previous case report describing MOG-Ab-positive patients with MRI lesions similar to our cases. [8] This patient initially presented with fever and impaired consciousness, and repeated MRI showed extensive brainstem edema with significant involvement of the bilateral pontine brachium and pons. Antiviral therapy was given on suspicion of acute meningitis, but nystagmus and quadriplegia with brain stem encephalitis rapidly developed over the next week.…”

Section: Discussionmentioning

confidence: 92%

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Bilateral pontine brachium lesions in one autoantibodies directed against MOG positive patient: A case report

Sun,

Shen,

Ding

et al. 2024

Medicine

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Rationale: Myelin oligodendrocyte glycoprotein (MOG) antibody-related disease is a relatively recent entity in inflammatory demyelinating disease. Its clinical presentation varies in severity and the lack of specific imaging features makes it easy to misdiagnose. We now report the case of a MOG antibody-positive patient who presented with diplopia and dizziness, and whose brain magnetic resonance imaging (MRI) showed abnormal signals in the bilateral pontine brachium. Patient concerns: A previously healthy 52-year-old woman presented with diplopia and dizziness, and was hospitalized 4 days after onset. Diagnoses: Brain MRI demonstrated abnormal hyperintense signals in the bilateral pontine brachium on T2-weighted fluid attenuated inversion recovery imaging. MRI enhancement showed abnormal enhancement foci in bilateral pontine brachium and pons. Cerebrospinal fluid examination showed Oligoclonal IgG bands were negative. The IgG index was normal, and serum aquaporin-4 antibody was negative, while serum MOG-Ab was positive (1:100). In conjunction with a positive serum MOG antibody and exclusion of other diseases, diagnosis of MOG antibody-related disease was made. Interventions: Intravenous methylprednisolone followed by oral corticosteroids. Outcomes: Symptoms resolved completely. At 4-month follow-up. Follow-up after 4 months showed disappearance of the abnormal signal in the left pontine brachium and diminution of abnormal high signal in the right compared to the previous one, and there was no recurrence 1 year after the onset of the disease. Lessons: If brain MRI indicating bilateral, multiple, and diffuse abnormal signals in the pontine brachium, and a discrepancy between the clinical symptoms and the imaging severity, a diagnosis of demyelinating disease should be considered highly probable. In such cases, anti-MOG antibody testing is essential for further defining the etiology. The clinical phenotype and imaging manifestations of MOG antibody-positive brainstem encephalitis may lack sufficient specificity to be readily identifiable. Timely diagnosis and early glucocorticoid therapy are beneficial in improving prognosis and preventing recurrence.

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Section: Discussionmentioning

confidence: 92%

“…[10] Olbert et al's case report highlights the potential for relapse and disease progression in MOGAD patients. [8] In this case, glucocorticoids were administered early in the course of the disease to patient who had mild clinical symptoms and a low serum MOG antibody titer. This effectively delayed the progression of the disease.…”

Section: Discussionmentioning

confidence: 99%