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To the Editor: A 7-y-old boy presented with a 3-d history of fever, headache, lethargy, vomiting, and a generalized tonic–clonic seizure on day 3 of illness, without prodromal systemic symptoms. He had neck stiffness on examination, and demonstrated irritability and excessive sleepiness with no cranial nerve or motor deficits. Blood showed neutrophilic leukocytosis (18000 WBCs/mm3, 55% neutrophils) and elevated C-reactive protein (CRP) (45 mg/dL). CSF showed 35 cells with a predominance of polymorphs with normal glucose (61 mg/dL) and protein (25 mg/dL). CSF gram stain, culture, and multiplex PCR (bacterial DNA, HSV-1 and 2, VZV, HHV-6, and 7 DNA, enterovirus RNA) were negative. The contrast-enhanced MRI of the brain was normal. The serum anti-MOG antibody was strongly positive (cell-based assay, indirect immunofluorescence). He improved with a course of IVIg (2 g/kg) and oral prednisolone (2 mg/kg followed by a gradual taper), and was discharged in 2 wk.
The spectrum of MOG antibody–associated disease (MOGAD) is rapidly expanding. Initially described as a major cause of acute disseminated encephalomyelitis (ADEM) with predominant white matter involvement, this antibody has been associated with isolated cortical encephalitis, and more recently, MRI-negative acute neurological syndromes including myelitis and encephalitis [1]. MRI-negative aseptic meningitis presentation of MOGAD is a recently recognized syndrome, adding to the widening clinical spectrum of this disorder [2]. Interestingly, in this entity, serum inflammatory markers are raised, with CSF often showing a neutrophilic leukocytosis, frequently raising suspicion of bacterial meningitis [3]. This prompted us to use IVIg initially instead of pulse steroids until culture results and anti-MOG titers were known. It has been hypothesized that the aseptic meningitis phase reflects a possible virus-induced disruption of the blood–brain barrier and subsequent trigger of anti-MOG antibody production, which may evolve into a demyelinating syndrome with changes detectable on MRI if left untreated [4].
References
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Song X, Ma J, Li X, Jiang L. Children suspected of having intracranial infection with normal brain magnetic resonance imaging may be associated with the myelin oligodendrocyte glycoprotein antibody. Brain Dev. 2022;44:281–6.
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Gombolay GY, Gadde JA. Aseptic meningitis and leptomeningeal enhancement associated with anti-MOG antibodies: A review. J Neuroimmunol. 2021;358:577653.
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Kesavan, S., Chari, A., Kandasamy, S. et al. MRI-Negative MOG Antibody-Associated Disease in Meningitis. Indian J Pediatr 90, 200 (2023). https://doi.org/10.1007/s12098-022-04419-2
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DOI: https://doi.org/10.1007/s12098-022-04419-2