A 38-year-old right-handed female nurse presented on 23rd December 2024 with an acute febrile illness characterized by fever, chills, vomiting, photophobia, and neck stiffness following a night shift. There was no associated rash, myalgia, or arthralgia. Cerebrospinal fluid analysis revealed a white blood cell count of 450 cells/mm³ with 70% lymphocytic predominance and elevated protein of 1.03 g/L, BioFire panel was negative. MRI of the brain demonstrated non contrast enhancing bilateral thalamic hyperintensitieson T2. She was empirically treated with intravenous ceftriaxone, vancomycin, and acyclovir for presumed infectious meningoencephalitis.
Over the following days, she developed progressive neurological symptoms including gait ataxia, urinary retention, and fecal incontinence without perineal sensory loss or paresthesia. Repeat MRI showed interval improvement in thalamic lesions but revealed new signal non enhancing abnormalities in the cerebellar peduncles. In the context of evolving multifocal central nervous system involvement and negative infectious workup, an autoimmune demyelinating process was suspected. Serum testing confirmed positivity for MOG antibodies, establishing the diagnosis of MOG antibody-associated disease. She was treated with high-dose intravenous methylprednisolone, resulting in marked clinical improvement, followed by an oral steroid taper. A follow-up MRI at 20 days demonstrated near-complete resolution of previously noted abnormalities.