Subsequently, with further studies that included cell-based assays for detection of MOG antibodies, MOG-IgG seropositivity was associated with various other clinical phenotypes, including AQP4-IgG–seronegative NMOSD, optic neuritis (ON), transverse myelitis (TM), and non-ADEM encephalitis. reported the detection of antibodies directed against natively folded MOG in a subset of patients with ADEM but only rarely in patients with multiple sclerosis (MS) and the control group. Humoral immune responses involving MOG have been studied for decades in murine models of neuroinflammation (e.g., experimental autoimmune encephalomyelitis), but convincing data regarding an association of autoantibodies targeting MOG and human disease were lacking until 2007. These patients were shown to produce IgG antibodies to myelin oligodendrocyte glycoprotein (MOG), which is expressed on the outer lamellae of myelin sheaths and oligodendrocytes in the CNS. With the increased scrutiny of acute disseminated encephalomyelitis (ADEM) and neuromyelitis optica spectrum disorder (NMOSD), researchers found patients who had symptoms typically seen with those disorders but who were negative for the aquaporin-4 (AQP4) antibodies (characteristic of NMOSD). Keywords: brain, MOGAD, MRI, multiple sclerosis, myelin oligodendrocyte glycoprotein antibody–associated disease, neuromyelitis optica spectrum disorder, orbit, spine Early accurate diagnosis of MOGAD is important because prognosis and treatment differ from those for NMOSD and MS. Spinal involvement is seen as longitudinally extensive transverse myelitis with a sagittal T2-hyperintense intramedullary spinal line, the axial “H” spinal cord sign (central cord gray matter T2 hyperintensity), and conus medullaris involvement. Intraorbitally, one sees edematous, enlarged, tortuous optic nerve or nerves bilateral long-segment T2 hyperintensity of anterior segments of the optic nerve sparing of the optic chiasm and retrochiasmatic pathways and perioptic nerve sheath and surrounding orbital fat enhancement. Intracranial features that suggest MOGAD include childhood acute disseminated encephalomyelitis pattern with diffuse signal abnormality in the cortical gray matter, subcortical white matter, deep white matter, and deep gray matter on T2-weighted and FLAIR images few bilateral T2-hyperintense fluffy and poorly demarcated lesions pontine or thalamic involvement (or both) and cerebellar peduncle lesions in children. We highlight the imaging characteristics of MOGAD and contrast them with neuromyelitis optica spectrum disorder (NMOSD) and multiple sclerosis (MS). Myelin oligodendrocyte glycoprotein antibody–associated disease (MOGAD) is a distinct CNS inflammatory disease with symptoms and imaging findings that overlap other neuroinflammatory disorders.
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