RESUMO
We report two distinct challenging initial presentations of myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD). Case 1 describes a 12-year-old boy who developed headaches refractory to pain medication followed by cranial neuropathies and intracranial hypertension, confirmed by lumbar puncture with an opening pressure >36 cm H2O. Case 2 describes a 3-year-old boy who developed new-onset seizures refractory to antiseizure medications, a presentation of FLAIR-hyperintense lesions in MOG-antibody associated encephalitis with seizures (FLAMES). On repeat magnetic resonance imaging, both patients were found to have cortical T2 hyperintensities, leptomeningeal contrast enhancement, and bilateral optic nerve enhancement. In the cerebrospinal fluid, both patients had CSF pleocytosis with neutrophilic predominance. The patients were treated with intravenous immunoglobulins, plasma exchange, and high-dose corticosteroids. The first patient achieved disease remission, whereas the second patient required the addition of rituximab for management of seizures. The two cases highlight the pleomorphic clinical phenotypes of MOGAD.
RESUMO
Acute disseminated encephalomyelitis is reported in a 14-year-old male patient associated with a pleural empyema caused by an esophageal perforation. During the hospital course, the patient experienced an episode of cardiac arrest, raising the question of hypoxic-ischemic cerebral injury, but the magnetic resonance imaging (MRI) findings and clinical course were most consistent with acute disseminated encephalomyelitis. After a course of methylprednisolone, broad-spectrum antibiotics, and bilateral chest tube placement, the patient recovered with only mild residual deficits, along with resolution of his MRI findings.