Atypical Anti-MOG syndrome with aseptic meningoencephalitis and pseudotumor cerebri-like presentations

Narayan, Ram; Wang, Cynthia; Sguigna, Peter V.; Husari, Khalil S.; Greenberg, Benjamin

doi:10.1016/j.msard.2018.10.003

Cited by 53 publications

(36 citation statements)

References 2 publications

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“…Optic disc edema is rare in MS or NMOSD but is present in up to 86% of patients with MOGAD-ON ( 13 , 21 , 22 , 24 , 26 , 27 ). Rarely, bilateral ON with disc edema can be mistaken for idiopathic intracranial hypertension especially if the patient also complains of headache and has elevated opening pressure on lumbar puncture; however lymphocytic pleocytosis in CSF and enhancement of optic nerve on orbital MRI point toward an inflammatory etiology and should prompt testing for MOG-Ab ( 28 ). Fulminant disc edema with peripapillary hemorrhages and “macular star” have been described in MOGAD-ON ( 29 – 31 ).…”

Section: Optic Neuritis and Other Visual Pathway Presentationsmentioning

confidence: 99%

The Expanding Clinical Spectrum of Myelin Oligodendrocyte Glycoprotein (MOG) Antibody Associated Disease in Children and Adults

Parrotta¹,

Kister

2020

Front. Neurol.

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Section: Optic Neuritis and Other Visual Pathway Presentationsmentioning

confidence: 99%

The Expanding Clinical Spectrum of Myelin Oligodendrocyte Glycoprotein (MOG) Antibody Associated Disease in Children and Adults

Parrotta¹,

Kister

2020

Front. Neurol.

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“…However, MOG-IgG syndrome may be associated with a wide spectrum of symptoms. Of note, meningoencephalitis was recently reported in a MOG-IgG syndrome case [3]. We report a Chinese patient with recurrent ON at disease initiation, who had a delayed diagnosis of MOG-IgG syndrome until recurrent meningoencephalitis appeared and serum MOG-IgG was detected.…”

Section: Introductionmentioning

confidence: 76%

“…Though our patient did not have clinical manifestations of infection such as upper respiratory tract or gastrointestinal symptoms, isolated fever may still easily be mistaken for precursor infection and may often be ignored. Headache, nausea, and vomiting accompanied by elevated CSF leukocytes suggest meningoencephalitis, which has recently been described in MOG-IgG syndrome [3], but they are rarely reported in MS. Although nausea/vomiting is the manifestation of area postrema syndrome in NMOSD, this core clinical characteristic requires a lesion in the area postrema, and therefore nausea/vomiting without a lesion in area postrema could not be explained by NMOSD.…”

Section: Discussionmentioning

confidence: 99%

Relapsing optic neuritis and meningoencephalitis in a child: case report of delayed diagnosis of MOG-IgG syndrome

et al. 2019

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Background Recurrent optic neuritis (ON) was previously thought to be associated with multiple sclerosis (MS) and neuromyelitis optica spectrum disorders (NMOSD). Meningoencephalitis has recently been suggested to be a clinical finding typical of myelin oligodendrocyte glycoprotein (MOG) encephalomyelitis. We report a Chinese patient with recurrent ON at disease initiation, who had a delayed diagnosis of MOG-IgG syndrome, until recurrent meningoencephalitis appeared and serum MOG-IgG was detected. Case presentation From the age of 7 years, an AQP4-IgG negative female patient had 10 disease recurrences, including 4 episodes of recurrent ON, 4 episodes of fever and meningoencephalitis, and 2 episodes of ON as well as meningoencephalitis. She was initially diagnosed as recurrent ON and treated with glucocorticoids followed by gradual tapering when ON reoccurred. Later, she was diagnosed as central nervous system infection when fever and meningoencephalitis appeared, and antiviral drugs and glucocorticoids were used. However, when she returned to our department for follow-up on July 2017, the results of serum demyelinating autoimmune antibody revealed positive MOG-IgG (titer 1:320 by an in-house, cell-based assay using live cells transfected with full-length human MOG). A diagnosis of MOG-IgG syndrome was established. Conclusions Testing for MOG-IgG in atypical MS and NMOSD patients, and patients with meningoencephalitis with a history of relapsing demyelinating symptoms is warranted. Electronic supplementary material The online version of this article (10.1186/s12883-019-1324-4) contains supplementary material, which is available to authorized users.

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“…Leptomeningeal enhancement can occur in MOG antibody–associated disorder, including spinal leptomeningeal enhancement, 6 and aseptic meningitis with demyelinating lesions. 7,8 MOG antibodies are more likely to occur in children as compared to adults. 1 Moreover, phenotypic presentations are different as children are more likely to present with encephalopathy or acute disseminated encephalomyelitis, whereas adults are more likely to have optic neuritis-myelitis.…”

Section: Discussionmentioning

confidence: 99%

Rate of Leptomeningeal Enhancement in Pediatric Myelin Oligodendrocyte Glycoprotein Antibody–Associated Encephalomyelitis

et al. 2021

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Introduction: Myelin oligodendrocyte glycoprotein antibodies (MOG-abs) are associated with demyelinating diseases. Leptomeningeal enhancement occurs in 6% of adult MOG-abs patients but rates in pediatric MOG-abs patients are unknown. Methods: Retrospective review of pediatric MOG-abs patients was performed. Results: Twenty-one patients (7 boys, 14 girls) were included with an average age of 8.6 years (range 2-15 years). Seven of 21 (33%) pediatric MOG-abs patients had leptomeningeal enhancement. Two patients’ relapses were manifested by leptomeningeal enhancement alone and another patient presented with seizures, encephalopathy, and aseptic meningitis without demyelinating lesions. Cerebrospinal fluid pleocytosis was seen in both leptomeningeal (4/7 patients) and nonleptomeningeal enhancement (10/14 patients). Interestingly, 3 patients with leptomeningeal enhancement had normal cerebrospinal fluid white blood cell count. Cortical edema was more likely in patients with leptomeningeal enhancement ( P = .0263). Conclusion: We expand the clinical spectrum of anti-MOG antibody–associated disorder. Patients with recurrent leptomeningeal enhancement without demyelinating lesions should be tested for MOG antibodies.

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Atypical Anti-MOG syndrome with aseptic meningoencephalitis and pseudotumor cerebri-like presentations

Cited by 53 publications

References 2 publications

The Expanding Clinical Spectrum of Myelin Oligodendrocyte Glycoprotein (MOG) Antibody Associated Disease in Children and Adults

The Expanding Clinical Spectrum of Myelin Oligodendrocyte Glycoprotein (MOG) Antibody Associated Disease in Children and Adults

Relapsing optic neuritis and meningoencephalitis in a child: case report of delayed diagnosis of MOG-IgG syndrome

Rate of Leptomeningeal Enhancement in Pediatric Myelin Oligodendrocyte Glycoprotein Antibody–Associated Encephalomyelitis

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