Dr. Birca et al. reported a case of a 15-year-old adolescent boy who presented with acute-onset encephalopathy after a viral prodrome and was found to have frequent, dramatic yawning without electroencephalographic correlation and without focal deficits. The patient had elevated protein in the CSF without pleocytosis and bilateral brainstem, asymmetric insular, and cranial nerve T2 hyperintensities on brain MRI. He improved after treatment with methylprednisolone and was diagnosed with acute disseminated encephalomyelitis (ADEM). In response, Drs. Fujimori and Nakashima cite their previous report of a 20-year-old man with antimyelin oligodendrocyte glycoprotein (MOG) antibody-associated brainstem encephalitis who also presented with pathologic frequent yawning in addition to other brainstem symptoms. They suggest that serum MOG-immunoglobulin G (IgG) status should also be determined in the case by Dr. Birca et al., given that nearly half of pediatric patients with ADEM are MOG-IgG seropositive. Responding to these comments, senior author Dr. Myers agrees that anti-MOG-IgG testing is appropriate in cases of suspected ADEM and notes that a broad inflammatory and infectious workup was ordered on both serum and CSF for their patient, with lumbar puncture being repeated 5 days after initial presentation. Reviewing the results of CSF testing for their patient, Dr. Myers notes that there was an elevated IgG index, and oligoclonal bands on one sample, but whereas antiaquaporin-4 antibody testing was negative, they were unable to test for anti-MOG antibodies because of a laboratory registration error. As Mycoplasma pneumoniae immunoglobulin M was positive in the serum, mycoplasma infection was believed to be the most likely trigger for the patient’s ADEM. This exchange highlights our evolving understanding of both the clinical manifestations and potential underlying etiologies of ADEM.