Myelin oligodendrocyte glycoprotein antibody–associated disease mimicking meningoencephalitis with fever, brainstem involvement, and marked cerebrospinal fluid pleocytosis: a case report

Abstract

Case Presentation: A previously healthy 21-year-old woman presented with urinary retention followed by diffuse paresthesia, severe headache, tremor, diplopia, and a febrile episode. She initially received antibiotics for presumed urinary tract infection without improvement. On admission, she was alert and oriented. Neurological examination showed horizontal nystagmus with variable fast phase and superficial hypoesthesia with a sensory level at T6. Muscle strength was preserved, with diffuse hyperreflexia. No meningeal signs were observed. Brain computed tomography was unremarkable. Cerebrospinal fluid analysis demonstrated marked lymphocytic pleocytosis (256 cells/mm³, 92% lymphocytes), mildly elevated protein, and normal glucose. Infectious investigation, including cultures and molecular tests, was negative. Brain magnetic resonance imaging showed T2/FLAIR hyperintensities involving the dorsal pons and medulla, including the area postrema, without diffusion restriction or contrast enhancement. Given the inflammatory pattern and negative infectious workup, autoimmune demyelinating disease was suspected. Serum testing revealed positive anti–myelin oligodendrocyte glycoprotein (MOG) antibodies (titer 1:10), while aquaporin-4 antibodies were negative. High-dose intravenous methylprednisolone was administered for five days, followed by oral corticosteroids. The patient improved clinically, and maintenance immunotherapy with azathioprine was initiated. At six-month follow-up, she remained neurologically asymptomatic with complete recovery. Discussion: Myelin oligodendrocyte glycoprotein antibody–associated disease (MOGAD) is an autoimmune inflammatory demyelinating disorder of the central nervous system with a heterogeneous spectrum. Optic neuritis and transverse myelitis are the most common manifestations, although brainstem syndromes, acute disseminated encephalomyelitis, and cortical encephalitis are also described. Cerebrospinal fluid abnormalities are frequent in MOGAD, with pleocytosis in more than half of patients. However, the median cell count is usually around 30–40 cells/mm³, and markedly elevated counts are uncommon. Such inflammatory profiles may resemble infectious meningitis or meningoencephalitis and lead to suspicion of neuroinfection. Brainstem involvement may occur in MOGAD, manifesting with diplopia, ataxia, or cranial nerve deficits. Magnetic resonance imaging may demonstrate lesions involving the dorsal brainstem, including the pons and medulla.This case illustrates an atypical presentation of MOG antibody–associated disease with brainstem involvement and marked cerebrospinal fluid pleocytosis, initially suggesting central nervous system infection. Final Comments: MOG antibody–associated disease may rarely mimic meningoencephalitis with fever and marked cerebrospinal fluid pleocytosis; early recognition enables timely immunotherapy.